最新刊期
卷 32 ， 期 20 ， 2026
- 摘要：ObjectiveTo investigate the effects and mechanisms of Fangji Fulingtang （FFD） on mitochondrial function in the mouse model of myocardial fibrosis （MF）.MethodsSixty SPF-grade male C57BL/6J mice were randomly allocated into six groups （n=10 per group）： control， model， low-dose， medium-dose， and high-dose （3.315， 6.63， and 13.26 g·kg-1， respectively） FFD， and captopril （20 mg·kg-1）. MF was induced by subcutaneous injection of isoproterenol （10 mg·kg-1·d-1） in other groups except the control group for 14 consecutive days， with simultaneous gavage of corresponding drugs. Left ventricular ejection fraction （LVEF） and left ventricular fractional shortening （LVFS） were measured by echocardiography. Serum levels of creatine kinase-MB （CK-MB）， cardiac troponin I （cTnI）， N-terminal pro-brain natriuretic peptide （NT-pro BNP）， tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， and interleukin-6 （IL-6） were determined by enzyme-linked immunosorbent assay （ELISA）. Malondialdehyde （MDA）， superoxide dismutase （SOD）， and glutathione （GSH） levels were measured by biochemical assays. Reactive oxygen species （ROS） were detected by dihydroethidium （DHE） fluorescence staining. Hematoxylin-eosin （HE）， Masson's trichrome， and wheat germ agglutinin （WGA） staining were performed to evaluate myocardial structure and fibrosis. Mitochondrial ultrastructure and function were assessed by transmission electron microscopy， adenosine triphosphate （ATP） colorimetric assay， and JC-1 fluorescence staining. The protein levels of phosphorylated adenosine monophosphate-activated protein kinase α subunit （p-AMPKα）， AMPKα， peroxisome proliferator-activated receptor gamma coactivator-1α （PGC-1α）， mitofusin 2 （MFN2）， pyruvate kinase M2 isoform （PKM2）， lactate dehydrogenase A （LDHA）， and hypoxia-inducible factor 1 alpha （HIF-1α） were analyzed by Western blot.ResultsCompared with the control group， the model group exhibited decreased LVEF and LVFS， increased heart weight index and heart weight-to-tibia length ratio （P<0.01）， elevated levels of myocardial injury markers （CK-MB， cTnI， and NT-pro BNP）， inflammatory cytokines （TNF-α， IL-1β， and IL-6）， and MDA， along with reduced SOD and GSH levels （P<0.01）. Enhanced interstitial collagen deposition and cardiomyocyte hypertrophy were observed in the model group （P<0.01）. Transmission electron microscopy and JC-1 staining revealed mitochondrial swelling， crista disruption， decreased ATP content， and reduced red/green fluorescence ratio in the model group （P<0.01）. Western blot analysis demonstrated downregulation of p-AMPKα， PGC-1α， and MFN2 and upregulation of PKM2， LDHA， and HIF-1α in the model group （P<0.01）. Compared with the model group， treatment with FFD or captopril improved LVEF and LVFS， reduced heart weight index and heart weight-to-tibia length ratio （P<0.05， P<0.01）， lowered the serum levels of CK-MB， cTnI， NT-pro BNP， TNF-α， IL-1β， IL-6， and MDA， increased the SOD and GSH levels （P<0.05， P<0.01）， attenuated the myocardial fibrosis and cardiomyocyte hypertrophy （P<0.01）， and restored the mitochondrial ultrastructure. The medium and high-dose FFD groups as well as the captopril group showed increased ATP production and red/green fluorescence ratio （P<0.05， P<0.01）. Furthermore， FFD upregulated the expression of p-AMPKα and PGC-1α while downregulating the expression of LDHA and HIF-1α （P<0.05， P<0.01）.ConclusionFFD activates the AMPK/PGC-1α/MFN2 signaling pathway and inhibits the PKM2/LDHA/HIF-1α axis to restore mitochondrial function and energy metabolic homeostasis， thereby attenuating isoproterenol-induced myocardial fibrosis.关键词：Fangji Fulingtang;myocardial fibrosis;mitochondrial function;adenosine monophosphate-activated protein kinase （AMPK）/peroxisome proliferator-activated receptor gamma coactivator 1-alpha （PGC-1α）/mitofusin 2 （MFN2）-pyruvate kinase M2 isoform （PKM2） signaling pathway;energy metabolism15|7|0更新时间：2026-09-16
- 摘要：ObjectiveTo investigate the protective effect of Qiju Dihuang Wan on diabetic retinopathy （DR） and its regulatory mechanism on the NOD-like receptor protein 3/Cysteinyl aspartate-specific proteinase-1/Gasdermin D （NLRP3/Caspase-1/GSDMD） signaling pathway.MethodsHuman retinal microvascular endothelial cells （HRMEC） were divided into the blank group， model group， and Qiju Dihuang Wan low- and high-dose groups. Except for the blank group， all groups were induced with 40 mmol·L-1 high glucose， and the treatment groups were supplemented with 6% and 12% Qiju Dihuang Wan-containing serum， respectively， based on the induction. After 24 h of culture， the levels of interleukin （IL）-1β and IL-18 were measured by enzyme-linked immunosorbent assay （ELISA）， pyroptosis-related protein expression was detected by immunofluorescence and Western blot， and the mRNA levels of NLRP3/Caspase-1/GSDMD signaling pathway-related molecules were determined by real-time polymerase chain reaction （Real-time PCR）. The mice were randomly divided into the blank group， model group， Qiju Dihuang Wan low-， medium-， and high-dose groups （11， 22， 44 g·kg-1·d-1）， and calcium dobesilate group （0.13 g·kg-1·d-1）. Except for the blank group， all groups were intraperitoneally injected with streptozotocin to establish the DR model. After successful modeling， the treatment groups received corresponding doses of Qiju Dihuang Wan crude drug or calcium dobesilate suspension by gavage once daily， while the blank group and model group received an equal volume of normal saline， for 8 consecutive weeks. Fundus changes were examined by optical coherence tomography， optical coherence tomography angiography， and fundus fluorescein angiography. Retinal pathological morphology was observed by hematoxylin-eosin staining. Real-time PCR was used to detect the mRNA levels of NLRP3， Caspase‑1， GSDMD， IL‑1β， and IL‑18 in retinal tissue， and Western blot was used to detect the protein expression of NLRP3， ASC， cleaved Caspase‑1， and GSDMD‑N.ResultsCell experiments showed that compared with the blank group， the model group showed significantly decreased HRMEC viability （P<0.01）， and significantly increased levels of IL-1β， IL-18， as well as increased protein expression of NLRP3， cleaved Caspase-1， and GSDMD-N （P<0.01）. Compared with the model group， the above indicators were significantly reduced in the high-dose Qiju Dihuang Wan groups （P<0.05， P<0.01）. Animal experiments showed that compared with the blank group， the model group had elevated blood glucose （P<0.01）， decreased retinal thickness and vascular density （P<0.01）， up‑regulated mRNA expression of NLRP3， Caspase‑1， GSDMD， IL‑1β and IL‑18 in retinal tissue （P<0.01）， and up‑regulated protein expression of NLRP3， ASC， cleaved Caspase‑1 and GSDMD‑N （P<0.01）. Compared with the model group， the Qiju Dihuang Wan medium- and high‑dose groups showed decreased blood glucose （P<0.01）， increased retinal thickness and vascular density （P<0.01）， alleviated retinal pathological damage， and down‑regulated mRNA expression of NLRP3， Caspase‑1， GSDMD， IL‑1β， IL‑18， as well as protein expression of NLRP3， ASC， cleaved Caspase‑1， and GSDMD‑N （P<0.05， P<0.01）.ConclusionQiju Dihuang Wan may exert protective effects against diabetic retinopathy by inhibiting the activation of the NLRP3/Caspase-1/GSDMD signaling pathway and alleviating high glucose-induced retinal pyroptosis.关键词：Qiju Dihuang Wan;diabetic retinopathy;pyroptosis;NOD-like receptor family pyrin domain containing 3 （NLRP3） inflammasome;human retinal microvascular endothelial cell13|2|0更新时间：2026-09-16
- 摘要：ObjectiveTo investigate the mechanisms of Zuojinwan in the treatment of colorectal cancer from the perspective of inhibiting M2 polarization of tumor-associated macrophages.MethodsA colorectal cancer mouse model was established by azoxymethane （AOM）/dextran sulfate sodium （DSS）. Body weight was recorded， disease activity index （DAI） and tumor number were calculated， and hematoxylin-eosin （HE） staining was used to observe colonic pathological changes. Enzyme-linked immunosorbent assay （ELISA） was used to detect the levels of interleukin-6 （IL-6）， transforming growth factor-β （TGF-β）， interleukin-1β （IL-1β）， and tumor necrosis factor-α （TNF-α） in colonic homogenates. Immunohistochemistry was used to detect proliferating cell nuclear antigen （PCNA） expression in the colon， and immunofluorescence was used to detect mannose receptor （CD206） expression in macrophages. In vitro， M2 macrophages were induced using IL-4/IL-13， and macrophages were treated with different concentrations of Zuojinwan-containing serum. CD206 and differentiation cluster 86 （CD86） were analyzed by flow cytometry. A CT26 and RAW264.7 macrophage co-culture system was established， and the migration and proliferation abilities of CT26 cells were detected using Transwell assays and trypan blue exclusion. Finally， proteomics was used to screen key proteins and signaling pathways involved in Zuojinwan-mediated inhibition of M2 polarization of tumor-associated macrophages in colorectal cancer， and Western blot was used for validation.ResultsIn animal experiments， compared with the blank group， mice in the model group showed significantly decreased body weight （P<0.05）， significantly increased DAI scores （P<0.01）， and significantly increased tumor number （P<0.01）， with severe colonic carcinogenesis and lymphatic metastasis. The protein expression levels of PCNA and CD206 were significantly increased （P<0.01）， and the levels of IL-6， IL-1β， TNF-α， and TGF-β in colonic homogenates were significantly increased （P<0.01）. Compared with the model group， mice in the Zuojinwan intervention group showed significantly higher body weight （P<0.05）， significantly decreased DAI scores （P<0.01）， and significantly reduced tumor numbers （P<0.01）. The protein levels of PCNA and CD206 were significantly decreased （P<0.05）， and the levels of IL-6， IL-1β， TNF-α， and TGF-β in colonic homogenates were significantly decreased （P<0.05）. In the CT26 and RAW264.7 co-culture system in vitro， compared with the blank group， co-culture with M2-type RAW264.7 macrophages significantly increased CT26 cell migration rate and proliferation number （P<0.01）. Compared with the M2 group （M2-type macrophages）， the proportion of CD86 was significantly increased in the Zuojinwan-containing serum group （P<0.01）， while the CT26 cell migration rate and proliferation number were significantly decreased in the 8% Zuojinwan-containing serum group （P<0.01）. Proteomics analysis indicated that tumor necrosis factor-α-induced protein 8-like protein 1 （TIPE1） may be a key target through which Zuojinwan regulates macrophage phenotypic transformation to inhibit colorectal cancer. The phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway showed the highest enrichment. Compared with the blank group， the levels of TIPE1， p-PI3K， and p-Akt in M2 macrophages were significantly increased （P<0.05，P<0.01）. After treatment with Zuojinwan-containing serum， the levels of TIPE1， p-PI3K， and p-Akt were significantly decreased （P<0.05，P<0.01）.ConclusionZuojinwan may inhibit colorectal cancer proliferation and migration by suppressing M2 polarization of tumor-associated macrophages， which may be associated with inhibition of the PI3K/Akt signaling pathway in tumor-associated macrophages.关键词：Zuojinwan;formula;colorectal cancer;tumor-associated macrophages;tumor necrosis factor-α-induced protein 8-like protein 1 （TIPE1）/phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt）signaling pathway27|12|0更新时间：2026-09-16
- 摘要：ObjectiveTo investigate the effect and mechanism of Banxia Shumitang plus Zhizichi Tang （BZ） on PTEN-induced kinase 1 （PINK1）/Parkin signaling pathway in regulating mitochondrial autophagy in preventing insomnia with depression.MethodsSeventy-two 6-week-old male Kunming mice were randomized into a normal group， a model group， low-dose， medium-dose， and high-dose BZ groups （BZ-L， BZ-M， BZ-H， 2.92， 5.85， 11.7 g·kg-1）， and an estazolam （0.21 mg·kg-1） group. Insomnia model was established on days 1 to 3. p-Chlorophenylalanine （PCPA） was injected intraperitoneally at a dose of 400 mg·kg-1 into mice of the model group and administration groups for 3 consecutive days. Then， the classic depression model was established with chronic unpredictable mild stress （CUMS） for 28 consecutive days. Administration and modeling were performed simultaneously. After gavage， 24 h spontaneous activity test was performed to test sleep state， and sugar preference test and open field test were performed to evaluate anxiety-like state. The morphological changes of the hypothalamus were observed by hematoxylin-eosin （HE） staining， and the number of Nissl bodies was observed by Nissl staining. The ultrastructure of mitochondria was observed by transmission electron microscopy. The mitochondrial membrane potential assay kit （JC-1） was used to examine the mitochondrial function， and a biochemical assay kit was used to measure the ATP content in the hypothalamus. The level of reactive oxygen species （ROS） was determined by the immunofluorescence assay， and the serum levels of 5-hydroxytryptamine （5-HT）， noradrenalin （NE）， and cortisol （CORT） were determined by enzyme-linked immunosorbent assay （ELISA）. Western blot and Real-time quantitative polymerase chain reaction （Real-time PCR） were employed to determine the expression of PINK1， Parkin， microtubule-associated protein 1 light chain 3 （LC3）， and isolator protein 1 （p62） at protein and mRNA levels， respectively.ResultsThe 24 h spontaneous activity test showed that compared with the normal group， the model group did not exhibit circadian rhythm characteristics in their spontaneous activity time， while the circadian rhythm characteristics were restored in each treatment group （P<0.05）. The sucrose preference test indicated that compared with that in the normal group， the sucrose preference rate in the model group reduced （P<0.01）， and compared with that in the model group， the sucrose preference rate in each treatment group increased （P<0.01）. The open field test revealed that compared with the normal group， the model group exhibited decreased movement distance， average speed， frequency of visits to the central area， and time spent in the central area （P<0.01）， and compared with those in the model group， these parameters in each treatment group increased （P<0.05， P<0.01）. HE staining showed that compared with the normal group， the model group exhibited disarrangement of neurons in the hypothalamus， enlarged intercellular space， and severe nuclear condensation， while the degree of hypothalamic neuronal damage in each treatment group was alleviated. Nissl staining indicated that compared with the normal group， the model group demonstrated aggravated neuronal damage and increased damaged cells （P<0.01）. Compared with that in the model group， the number of damaged cells in each treatment group decreased （P<0.01）. Transmission electron microscopy showed that compared with the normal group， the model group exhibited mitochondrial swelling and rupture in the hypothalamus， with visible autophagic lysosomes in the cytoplasm. Compared with those in the model group， only a few autophagic lysosomes were observed in the BZ-L group， and the degree of mitochondrial swelling and rupture was alleviated in the other treatment groups. ROS immunofluorescence assay showed that compared with the normal group， the model group displayed enhanced red fluorescence intensity of mitochondrial ROS （P<0.01）， which was attenuated in each treatment group （P<0.01）. Mitochondrial membrane potential assay showed that compared with the normal group， the model group had declined mitochondrial membrane potential （P<0.01）， which was recovered in each treatment group （P<0.05， P<0.01）. The biochemical assay of ATP levels indicated that compared with the normal group， the model group exhibited decreased ATP content （P<0.01）， which rebound in each treatment group （P<0.05， P<0.01）. ELISA showed that compared with the normal group， the model group exhibited decreased 5-HT content and increased NE and CORT content （P<0.01）. Compared with the model group， each treatment group showed increased 5-HT content （P<0.01） and reduced NE content （P<0.01） and CORT content （P<0.05， P<0.01）. Western blot of the hypothalamus showed that compared with the normal group， the model group exhibited downregulated protein levels of PINK1， Parkin， and LC3 （P<0.01） and upregulated protein level of p62 （P<0.01）. Compared with the model group， each treatment group showed upregulated protein levels of PINK1， Parkin， and LC3 （P<0.05， P<0.01） and downregulated protein level of p62 （P<0.05， P<0.01）. Real-time PCR showed that compared with the normal group， the model group exhibited downregulated mRNA levels of PINK1， Parkin， and LC3 （P<0.01） and upregulated mRNA level of p62 （P<0.01）. Compared with the model group， each treatment group showed upregulated mRNA levels of PINK1， Parkin， and LC3 （P<0.01） and downregulated mRNA level of p62 （P<0.01）.ConclusionBZ can ameliorate the insomnia and anxiety state of mice by regulating PINK1/Parkin signaling pathway to improve the mitochondrial function， enhance mitochondrial autophagy， protect neurons， and repair damaged nerve cells.关键词：insomnia;depression;Banxia Shumitang;Zhizichi Tang;PTEN-induced kinase 1（PINK1）/Parkin signaling pathway;mitochondrial autophagy41|7|0更新时间：2026-09-16
- 摘要：ObjectiveTo observe the effects of modified Longdan Xiegan Tang on wound healing and inflammatory factors after surgery for perianal abscess of heat-toxin accumulation syndrome.MethodsA prospective randomized controlled design was adopted. A total of 110 patients with perianal abscess of heat-toxin accumulation syndrome admitted to Hebei Provincial Hospital of Traditional Chinese Medicine from January 2024 to January 2025 were included and randomly assigned into two groups， each with 55 patients according to the random number table method. The control group received conventional Western medicine treatment + placebo oral administration after surgery， and the observation group received modified Longdan Xiegan Tang oral administration on the basis of conventional Western medicine treatment， with a course of 14 days. Clinical efficacy， Visual Analogue Scale （VAS） score， wound secretion score， TCM symptom score， wound healing rate， wound healing time， wound infection rate， inflammatory factors ［interleukin-6 （IL-6）， interleukin-8 （IL-8）， and tumor necrosis factor-α （TNF-α）］， wound healing-related indicators ［fibronectin （FN）， matrix metalloproteinase-9 （MMP-9）， and prealbumin （PA）］ and adverse reactions were determined in both groups.ResultsThree cases in the observation group and three cases in the control group dropped out， with 104 cases actually completing the study. The repeated measures analysis of variance showed that both groups showed decreased VAS scores， wound secretion scores， TCM syndrome scores， and levels of IL-6， IL-8， TNF-α， and MMP-9 and increased levels of PA and FN after treatment （P<0.05）. During treatment and on day 14 after surgery， the observation group had lower VAS score， wound secretion score， TCM syndrome score， and levels of IL-6， IL-8， TNF-α， and MMP-9 and higher levels of PA and FN than the control group （P<0.01）. The observation group showed higher wound healing rate， shorter wound healing time， and lower wound infection than the control group （P<0.01）. The comprehensive efficacy of the observation group was better than that of the control group （χ2=5.216， P<0.05）. No serious adverse events occurred in patients during the study， and there was no significant difference in the incidence of adverse reactions between the two groups.ConclusionModified Longdan Xiegan Tang can ameliorate wound condition， reduce inflammatory response， and promote wound healing in patients with perianal abscess of heat-toxin accumulation syndrome after surgery， with good safety.关键词：modified Longdan Xiegan Tang;heat-toxin accumulation syndrome;perianal abscess;wound healing;inflammatory factors;Fibronectin57|13|0更新时间：2026-09-16
- 摘要：ObjectiveTo investigate the effect of Gardeniae Fructus-Salviae Miltiorrhizae Radix et Rhizoma on ferroptosis in the rat model of myocardial infarction and further elucidate its role in myocardial remodeling.MethodsThe rat model of myocardial infarction was established by ligation of the left anterior descending coronary artery. The 50 successfully modeled rats were randomly divided into model group， ferroptosis inhibitor group （2 mg·kg-1）， enalapril group （2.1 mg·kg-1）， and low- and high-dose （4 g·kg-1 and 8 g·kg-1， respectively） Gardeniae Fructus-Salviae Miltiorrhizae Radix et Rhizoma， with 10 rats in each group. The rat model of myocardial infarction was established by ligation of the left anterior descending coronary artery. After 4 weeks of treatment， echocardiography was used to assess the cardiac structure and function. Hematoxylin-eosin （HE） staining and Masson staining were employed to observe pathological morphology and fibrosis of the myocardial tissue. Serum levels of N-terminal pro-B-type natriuretic peptide （NT-proBNP）， transforming growth factor-β （TGF-β）， and myosin heavy chain-β （MHC-β） were measured by enzyme-linked immunosorbent assay （ELISA）. Prussian blue staining was performed to detect myocardial iron deposition. The myocardial mitochondrial structure was observed by transmission electron microscopy. Levels of malondialdehyde （MDA） and glutathione （GSH） in the myocardial tissue were determined by lipid peroxidation assay kits. Immunofluorescence assay was conducted to observe the fluorescence intensity of nuclear factor E2-related factor 2 （Nrf2） in the myocardial tissue. Western blot analysis was performed to evaluate the expression levels of proteins in the Nrf2/solute carrier family 7 member 11 （SLC7A11）/glutathione peroxidase 4 （GPX4） pathway.ResultsCompared with the sham group， the model group showed increased left ventricular end-diastolic diameter （LVEDD）， left ventricular end-systolic diameter （LVESD）， and serum levels of NT-proBNP， TGF-β， and MHC-β （P<0.01）， decreased left ventricular ejection fraction （LVEF） and left ventricular fractional shortening （LVFS） （P<0.01）， disarrangement of myocardial cells， inflammatory cell infiltration， severe myocardial fibrosis， increased myocardial iron deposition， and irregular mitochondrial morphology with vacuolation. Furthermore， the modeling led to increased MDA （P<0.01）， decreased GSH （P<0.01）， diminished Nrf2 fluorescence intensity in the myocardial tissue， and downregulated expression levels of Nrf2， SLC7A11， and GPX4 （P<0.01）. Compared with the model group， Gardeniae Fructus-Salviae Miltiorrhizae Radix et Rhizoma reduced the LVEDD， LVESD， and serum levels of NT-proBNP， TGF-β， and MHC-β （P<0.05， P<0.01）， increased the LVEF and LVFS （P<0.05， P<0.01）， alleviated pathological changes such as myocardial cell disarrangement， inflammatory cell infiltration， myocardial fibrosis， and iron deposition， lowered the level of MDA （P<0.05， P<0.01）， raised the level of GSH （P<0.05， P<0.01）， improved the mitochondrial morphology and reduced vacuolation in the myocardial tissue， enhanced Nrf2 fluorescence intensity， and upregulated the expression levels of Nrf2， SLC7A11， and GPX4 （P<0.05， P<0.01） in the rat model of myocardial infarction.ConclusionGardeniae Fructus-Salviae Miltiorrhizae Radix et Rhizoma alleviates pathological damage and myocardial remodeling in the rat model of myocardial infarction by inhibiting ferroptosis， the mechanism of which is related to the activation of Nrf2/SLC7A11/GPX4 signaling pathway.关键词：nuclear factor E2-related factor 2/solute carrier family 7 member 11/glutathione peroxidase 4 （Nrf2/SLC7A11/GPX4） signaling pathway;Gardeniae Fructus-Salviae Miltiorrhizae Radix et Rhizoma;ferroptosis;myocardial infarction;myocardial remodeling1|0|0更新时间：2026-09-16
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Exploring Pathogenesis and Treatment of Gastric Cancer Metastasis Based on Blood Harmonizing Method AI导读
摘要：Metastasis in gastric cancer is a key factor contributing to poor prognosis. Its pathogenesis is complex， characterized by a combination of underlying deficiency and superficial excess， cold and heat in complexity， and stagnation in collateral Conventional aggressive treatment methods tend to exacerbate the depletion of healthy Qi and Zang-Fu organ dysfunctions. The harmonizing method in traditional Chinese medicine （TCM） emphasizes holistic regulation and reinforcing healthy Qi while expelling pathogenic factors. The blood harmonizing method is grounded in the core TCM theory of blood vessel transmission and Zang-Fu organ accumulation of cancerous toxins. It closely addresses the essence of metastasis-where cancerous toxins spread through the bloodstream and accumulate in the collaterals-thereby providing a unique and feasible diagnostic and therapeutic approach for clinical intervention in gastric cancer metastasis. This paper systematically reviews relevant TCM theories such as transmission and Zang-Fu organ accumulation of cancerous toxins and accumulation-gathering and provides an in-depth explanation of the core pathogenesis of gastric cancer metastasis. Specifically， cancerous toxins circulate throughout the body via the blood vessels and accumulate in the collaterals of target organs such as the liver， peritoneum， lymph nodes， and lungs. The occurrence and development of this process are consistently centered on the key mechanism of disharmony in blood-related syndromes. On this basis， the paper explicitly proposes three major therapeutic approaches centered on harmonizing the blood. The first is harmonizing the blood to restore ascending and descending functions， thereby invigorating the spleen and regulating the middle energizer to restore the mediating function of the middle energizer and block the generation of phlegm and blood stasis at the root. The second is harmonizing the blood to balance cold and heat， using pungent herbs to open and bitter herbs to descend to harmonize the Yin-Yang balance and improve the homeostasis of the tumor microenvironment. The third is harmonizing the blood to unblock collaterals and resolve stasis， thereby gradually dissipating stasis and nodules， gently clearing obstructions in the collaterals， and breaking the critical link of collateral stagnation forming masses caused by metastasis. The article further summarizes modern pharmacological research findings on representative formulas such as Banxia Xiexintang， Weichang'an， Yangzheng Sanjie decoction， and Sijunzitang， confirming that they can inhibit the proliferation， invasion， and metastasis of gastric cancer cells， as well as epithelial-mesenchymal transition， through multiple targets and pathways， to regulate angiogenesis and lymphangiogenesis， modulate the immune microenvironment， and induce tumor cell apoptosis and ferroptosis， thereby blocking the metastasis process at multiple levels. This paper discusses the theoretical basis， pathogenetic mechanisms， therapeutic systems， and modern mechanisms of the blood harmonizing method for the diagnosis and treatment of gastric cancer metastasis. It fully embodies the TCM principles of targeting balance， reinforcing healthy Qi without aiding the pathogen， and eliminating the pathogen without harming the healthy Qi， providing a solid theoretical foundation and practical pharmacological references for the prevention and treatment of gastric cancer metastasis with integrated traditional Chinese and Western medicine in clinical practice.关键词：harmonizing blood;gastric cancer metastasis;peritoneal metastasis;blood vessels;therapeutic method34|7|0更新时间：2026-09-16 - 摘要：ObjectiveTo investigate the synergistic promotion of malignant phenotypes in gastric cancer cells by tumor-associated bone marrow mesenchymal stem cells （TA-BMSCs） and polymorphonuclear myeloid-derived suppressor cells （PMN-MDSCs） through crosstalk， and the intervention mechanism of the intestinal absorption solution containing Banxia Xiexintang （BXT）.MethodsGastric cancer MFC cells were treated with conditioned medium （co-culture-CM） prepared from a co-culture system of TA-BMSCs and PMN-MDSCs. Groups included control， co-culture-CM model， stromal cell-derived factor 1 （SDF1） inhibitor （LY2510924）， α4β1 inhibitor （BIO5192）， dual inhibitor combination， and different concentrations （55%， 70%， 85%） of BXT-containing intestinal absorption solutions. MFC cell proliferation， migration， invasion， and apoptosis were assessed via cell counting kit-8 （CCK-8） assay， wound-healing assay， Transwell assay， and flow cytometry. The SDF-1， α4β1， matrix metalloproteinase-9 （MMP-9）， and vascular endothelial growth factor A （VEGFA） levels in culture supernatants， along with the protein levels of intracellular macrophage migration inhibitory factor （MIF）， chemokine （C-X-C motif） receptor 4 （CXCR4）， CD106， MMP-9， and VEGFA in MFC cells， were measured by enzyme-linked immunosorbent assay （ELISA） and Western blot， respectively.ResultsCompared with the control group， co-culture-CM promoted the proliferation， migration， and invasion of MFC cells （P<0.01）， elevated the levels of SDF-1， α4β1， MMP-9， and VEGFA （P<0.01）， and upregulated the protein levels of MIF （P<0.05）， MMP-9 （P<0.01）， and VEGFA （P<0.01）. Compared with co-culture-CM， BXT-containing intestinal absorption solutions at various concentrations significantly reversed the phenotypic effects on cells， inhibited malignant phenotypes， lowered the levels of MMP-9 and SDF1， and reduced the expression of proteins in the crosstalk axis. Compared with the SDF1+α4β1 inhibitor group， the SDF1 inhibitor group and the α4β1 inhibitor group showed no differences in the inhibition of proliferation， scratch healing， and cytokine levels. The SDF1 inhibitor increased the apoptosis rate and downregulated the protein levels of MIF and CD106， while the α4β1 inhibitor increased the number of migrated cells and the expression of various proteins. Compared with the SDF1 inhibitor group， the α4β1 inhibitor group showed reduced inhibitory effect on proliferation， decreased apoptosis rate， increased number of invasive cells， decreased α4β1 content， and increased expression of various proteins （P<0.01）. The 55%， 70%， and 85% intestinal absorption solutions increased the inhibitory effect on proliferation， decreased the number of invasive cells， and increased the apoptosis rate （P<0.01）. The 55% BXT-containing intestinal absorption solution group showed increased wound healing rate and upregulated protein levels of VEGFA， CD106， and MMP-9 （P<0.05）. The 70% intestinal absorption solution group showed upregulated protein level of MIF （P<0.05）， and the 85% intestinal absorption solution group showed upregulated protein level of VEGFA （P<0.01） and downregulated the protein level of CXCR4 （P<0.01）.ConclusionTA-BMSCs and PMN-MDSCs synergistically activate the MIF/SDF-1/CXCR4 and MMP-9/α4β1/CD106 axes through crosstalk， significantly enhancing gastric cancer cell invasion and migration. BXT-containing intestinal absorption fluid effectively inhibits the malignant progression of gastric cancer cells by multi-targeted intervention in this crosstalk process.关键词：Banxia Xiexintang;drug-containing intestinal absorption solution;tumor-associated bone marrow mesenchymal stem cells;polymorphonuclear myeloid-derived suppressor cells;cell crosstalk43|9|0更新时间：2026-09-16
- 摘要：ObjectiveTo explore whether the intestinal absorption solution containing Banxia Xiexintang （BXT） can inhibit the invasion and migration of gastric cancer cells by interfering with the stromal cell-derived factor 1 （SDF1）-CXC chemokine receptor 4 （CXCR4） axis in tumor-associated bone marrow mesenchymal stem cells （TA-BMSCs）.MethodsThe intestinal absorption solution containing BXT was prepared， and the optimal intervention concentration and duration for MFC cells were determined through the cell counting kit-8 （CCK-8） assay. A co-culture system was established comprising TA-BMSCs conditioned medium （TA-BMSCs-CM） and gastric cancer MFC cells. The experiment was conducted with a blank control group， a TA-BMSCs-CM group， an SDF1 inhibitor （LY2510924） group， and intervention groups with varying concentrations （55%， 70%， 85%） of the intestinal absorption solution containing BXT. Cell proliferation was assessed by the CCK-8 assay. Horizontal and vertical cell migration were evaluated via scratch and Transwell assays， respectively. Cell invasion was examined by a Transwell assay with Matrigel. Cell apoptosis was detected by flow cytometry. The levels of factors such as SDF1， matrix metalloproteinase-9 （MMP-9）， and vascular endothelial growth factor A （VEGFA）， as well as the protein levels of macrophage migration inhibitory factor （MIF）， CXCR4， VEGFA， and MMP-9， were quantified by ELISA and Western blot， respectively.ResultsThe CCK-8 assay results indicated that compared with the 24 h intervention， the 48 h interventions with all concentrations of the intestinal absorption solution containing BXT increased the inhibition rate on MFC cells （P<0.01）. The half-maximal inhibitory concentration （IC50） of the intestinal absorption solution containing BXT at the time point of 48 h was 68.51%， and subsequent intervention concentrations were selected as 55%， 70%， and 85%. Compared with the TA-BMSCs-CM group， the intestinal absorption solution containing BXT （particularly at concentrations of 70% 85%） suppressed the proliferation， migration， and invasion of MFC cells， promoted the cell apoptosis （P<0.05， P<0.01）， decreased the levels of SDF1， MMP-9， and VEGFA， and downregulated the protein levels of MIF， CXCR4， VEGFA， and MMP-9 （P<0.05， P<0.01）. The inhibitory effects of the intestinal absorption solution containing BXT were comparable to or superior to those of the SDF1 inhibitor （P<0.01）.ConclusionThe intestinal absorption solution containing BXT can inhibit the invasion and migration of gastric cancer cells by interfering with the SDF1-CXCR4 axis in TA-BMSCs. The underlying mechanism may involve the regulation of the MIF/SDF1/CXCR4 signaling pathway and its downstream effector molecules.关键词：Banxia Xiexintang;drug-containing intestinal absorption solution;tumor-associated bone marrow mesenchymal stem cells;cell crosstalk42|12|0更新时间：2026-09-16
- 摘要：ObjectiveTo observe how Banxia Xiexintang affects programmed cell death 1 ligand 1 （PD-L1） expression induced by exosomes derived from gastric cancer cells in bone marrow mesenchymal stem cells （BMSCs） through the protein kinase B （Akt）/c-myelocytomatosis oncogene （c-Myc） signaling axis， and its effects on the migration of BMSCs and gastric cancer cells.MethodsExosomes were isolated from human gastric cancer NCI-N87 cells and identified by transmission electron microscopy and Western blot. Rat BMSCs were passaged and identified by immunofluorescence staining. A Transwell chamber was used to create a non-contact co-culture system for NCI-N87 exosomes and BMSCs. The experiment was designed with normal， model， Banxia Xiexintang （10% serum containing Banxia Xiexintang）， PD-L1 monoclonal antibody （10% blank serum containing PD-L1 antibody）， and combination （10% serum containing Banxia Xiexintang and 10% blank serum containing PD-L1 antibody） groups. The suspension of BMSCs was added to the upper chamber of each group， with the normal group receiving serum culture medium without exosomes in the lower chamber， and the model group receiving NCI-N87 exosomes. The Banxia Xiexintang group， PD-L1 monoclonal antibody group， and combination group received 10% serum containing Banxia Xiexintang， 10% blank serum containing PD-L1 monoclonal antibody， and 10% serum containing Banxia Xiexintang and 10% blank serum containing PD-L1 antibody， respectively， in the upper chamber. After 96 h， BMSCs from the upper chamber were collected， and the protein levels of p-Akt， Akt， c-Myc， and PD-L1， as well as the mRNA levels of Akt， c-Myc， and PD-L1， were determined by Western blot and Real-time PCR， respectively. The migration of BMSCs and NCI-N87 was assessed by the Transwell method.ResultsCompared with the normal group， the model group showed increases in protein levels of p-Akt， c-Myc， and PD-L1， as well as mRNA levels of c-Myc and PD-L1 （P<0.05， P<0.01）， and no significant change in the protein and mRNA levels of Akt. Compared with the model group， the Banxia Xiexintang group， PD-L1 monoclonal antibody group， and combination group showed decreases in protein levels of p-Akt， c-Myc， and PD-L1 （P<0.01）. In addition， they had significant effects on the protein and mRNA levels of Akt. The combination group showed greater reductions in the protein and mRNA levels of c-Myc and PD-L1 than the Banxia Xiexintang group and PD-L1 monoclonal antibody group （P<0.05）. Compared with the normal group， the model group showed increases in the number of migrating NCI-N87 and BMSCs （P<0.05， P<0.01）. Compared with the model group， the Banxia Xiexintang group， PD-L1 monoclonal antibody group， and combination group showed decreases in the number of migrating NCI-N87 and BMSCs （P<0.05， P<0.01）， with the combination group showing greater reductions in the number of migrating NCI-N87 and BMSCs than the Banxia Xiexintang group and PD-L1 monoclonal antibody group （P<0.01）.ConclusionBanxia Xiexintang can lower the PD-L1 expression induced by gastric cancer cell-derived exosomes in BMSCs induced and inhibit the migration of BMSCs and gastric cancer cells. Moreover， it has a synergistic effect when being used together with PD-L1， possibly related to the regulation of the Akt/c-Myc signaling axis.关键词：Banxia Xiexintang;gastric cancer cell-derived exosomes;bone marrow mesenchymal stem cells;protein kinase B （Akt）/c-mycmyelocytomatosis oncogene （c-Myc） signaling axis;programmed cell death 1-ligand 1 （PD-L1）33|10|0更新时间：2026-09-16
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Efficacy of Tanreqing Gel in Treating Acne and Its Effect on TLR2/MyD88/NF-
κ B Signaling Pathway AI导读摘要：ObjectiveTo explore the pharmacological mechanism of Tanreqing gel （TRQG） in the treatment of acne by regulating the Toll-like receptor 2 （TLR2）/myeloid differentiation 88 （MyD88）/nuclear factor-κB （NF-κB） signaling pathway.MethodsThe minimum inhibitory concentration （MIC） of Tanreqing injection （TRQ） against Cutibacterium acnes was determined through the microdilution broth method， and drug resistance induction experiments were conducted. A mouse model of acne was established through inoculation of C. acnes on the back. The effects of TRQG on skin structure， pustule formation， collagen repair， and inflammatory response were evaluated by dermoscopy， histopathology， two-photon excitation fluorescence microscopy （TPEF）， and optical coherence tomography （OCT）. Differentially expressed genes （DEGs） were identified through transcriptome sequencing and then subjected to KEGG pathway enrichment analysis. In the RAW264.7 cell model， the optimal dosage of TRQG was determined through cell viability assays. Subsequently， the expression of key proteins in the TLR2/MyD88/NF-κB pathway and downstream inflammatory factors ［tumor necrosis factor-α （TNF-α）， interleukin （IL）-1β， and IL-6］ was determined by Western blot and real-time PCR.ResultsThe MIC of TRQ against C. acnes was 4 125 mg·L-1. Although TRQ had weaker antibacterial activity than erythromycin （ERY） and fusidic acid （FA）， it was less likely to induce bacterial resistance. In vivo experiments showed that TRQG improved the skin structure， promoted collagen repair （P<0.01）， inhibited pustule formation （P<0.01）， alleviated follicular keratinization and sebaceous gland hyperplasia， and reduced inflammatory responses in the mouse model of acne compared with erythromycin gel （ERYG）. Transcriptome analysis suggested that the TLR/MyD88/NF-κB signaling pathway was a key enriched pathway. Further experimental validation indicated that TRQG inhibited the expression of TLR2， MyD88， TNF receptor-associated factor 6 （TRAF6）， phosphorylated （p）-transforming growth factor-β-activated kinase 1 （TAK1）， p-inhibitor of NF-κB subunit α （IκBα）， and p-NF-κB in this pathway （P<0.01）. Meanwhile， Real-time PCR results confirmed that TRQG reduced the mRNA levels of TNF-α， IL-1β， and IL-6 （P<0.01）.ConclusionTRQG exerts its therapeutic effect on acne by inhibiting the activation of the TLR2/MyD88/NF-κB signaling pathway and reducing the release of downstream inflammatory factors. Furthermore， it is less likely to induce bacterial resistance， indicating a promising application prospect.关键词：Tanreqing Gel;acne;Cutibacterium acnes;Toll-like receptor 2 （TLR2）/myeloid differentiation 88 （MyD88）/nuclear factor-κB （NF-κB） signaling pathway;anti-inflammatory mechanism36|11|0更新时间：2026-09-16 - 摘要：ObjectiveThis study aimed to evaluate the effects of cycloastragenol （CAG） on mitochondrial dysfunction during cardiac remodeling and to elucidate its regulatory role in myocardial energy metabolic homeostasis and the associated transcriptional regulatory axis.MethodsA rat model of heart failure （HF） was established by ligation of the left anterior descending coronary artery. Rats were randomly divided into a control group， a model group， a captopril group （3.25 mg·kg-1）， a low-dose CAG group （10 mg·kg-1， CAG-L）， and a high-dose CAG group （20 mg·kg-1， CAG-H）. After 28 days of treatment， left ventricular ejection fraction （LVEF）， left ventricular fractional shortening （LVFS）， left ventricular end-diastolic diameter （LVIDd）， and left ventricular end-systolic diameter （LVIDs） were assessed by echocardiography. Serum levels of N-terminal pro-brain natriuretic peptide （NT-proBNP）， creatine kinase-MB （CK-MB）， cardiac troponinⅠ （cTnI）， interleukin-1β （IL-1β）， interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， and cyclic adenosine monophosphate （cAMP） were measured by enzyme-linked immunosorbent assay （ELISA）. Hematoxylin-eosin （HE） and Masson's trichrome staining were used to evaluate myocardial histopathology and fibrosis. Wheat germ agglutinin （WGA）， reactive oxygen species （ROS）， and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling （TUNEL） staining were performed to assess cardiomyocyte hypertrophy， oxidative stress， and apoptosis. Adenosine triphosphate （ATP） content and the activities of mitochondrial respiratory chain complexes Ⅰ-Ⅳ were determined by colorimetric assays. The mRNA expression of α-smooth muscle actin （α-SMA）， Col Ⅰ， and Col Ⅲ was detected by Real-time quantitative polymerase chain reaction （Real-time PCR）， while the protein levels of β2-adrenergic receptor （ADRB2）， protein kinase A （PKA）， phosphorylated cAMP response element-binding protein/total cAMP response element-binding protein （p-CREB/CREB）， peroxisome proliferator-activated receptor γ coactivator-1α （PGC-1α）， nuclear respiratory factor 1 （NRF1）， and mitochondrial transcription factor A （TFAM） were analyzed by Western blot.ResultsCompared with the control group， the model group exhibited significantly decreased LVEF， LVFS， and ATP levels （P<0.05）， and markedly increased LVIDd， LVIDs， NT-proBNP， CK-MB， cTnI， IL-1β， IL-6， TNF-α， ROS levels， TUNEL-positive rate， Col deposition area， and the mRNA expression of α-SMA， Col Ⅰ， and Col Ⅲ （P<0.05）. In addition， the activities of mitochondrial respiratory chain complexes Ⅰ-Ⅳ， the protein expression of ADRB2， PKA， p-CREB， PGC-1α， NRF1， and TFAM， as well as the cAMP content， were significantly reduced （P<0.05）. Compared with the model group， both low- and high-dose CAG significantly increased LVEF and LVFS， and decreased LVIDd， LVIDs， and the levels of NT-proBNP， CK-MB， and cTnI （P<0.05）. CAG treatment alleviated myocardial disarray and Collagen deposition， and downregulated the mRNA expression of α-SMA， Col Ⅰ， and Col Ⅲ. The treatment markedly reduced ROS generation and the TUNEL-positive rate （P<0.05）， thereby attenuating cardiomyocyte hypertrophy and inflammatory responses. Furthermore， CAG treatment increased ATP content and the activities of mitochondrial respiratory chain complexes Ⅰ-Ⅳ， accompanied by upregulation of PGC-1α， NRF1， TFAM， ADRB2， PKA， and p-CREB protein expression as well as cAMP levels （P<0.05）. The CAG-H group showed the most pronounced improvements， which were superior to those of the captopril group and the CAG-L group.ConclusionCycloastragenol delays adverse cardiac remodeling and improves cardiac function by activating the ADRB2-mediated GPCR/cAMP/PKA/CREB signaling pathway， enhancing the PGC-1α/NRF1/TFAM activity， promoting mitochondrial energy metabolism remodeling， and suppressing oxidative stress， inflammation， and myocardial fibrosis.关键词：cycloastragenol;heart failure;G protein-coupled receptor/cyclic adenosine monophosphate/protein kinase A/cAMP response element-binding protein （GPCR/cAMP/PKA/CREB）;peroxisome proliferator-activated receptor γ coactivator-1α/nuclear respiratory factor 1/mitochondrial transcription factor A （PGC-1α/NRF1/TFAM）;mitochondrial function;cardiac remodeling39|8|0更新时间：2026-09-16
- 摘要：ObjectiveTo investigate the effects and potential mechanisms of Babaodan （BBD） against acetaminophen （APAP）-induced acute liver injury （ALI） based on transcriptomics.MethodsA total of 36 male C57BL/6 mice were randomly divided into 6 groups （n=6 per group）： normal group， model group， N-acetylcysteine group （NAC， 120 mg·kg-1）， and BBD low-， medium-， and high-dose groups （BBD-L， BBD-M， BBD-H groups， 75， 150， 300 mg·kg-1， respectively）. Except for the normal group， all other groups were subjected to APAP-induced ALI. The serum levels of aspartate aminotransferase （AST）， alanine aminotransferase （ALT）， total cholesterol （TC）， triglyceride （TG）， and low-density lipoprotein cholesterol （LDL-C） were measured in each group. Hepatic levels or activities of malondialdehyde （MDA） and glutathione peroxidase （GSH-Px） were detected using commercial kits. Hematoxylin-eosin （HE） staining was performed to evaluate the degree of liver histopathological damage. Transcriptomic analysis was employed to screen differentially expressed genes （DEGs）， and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis was performed to identify differential pathways involved in BBD intervention against ALI. Real-time quantitative polymerase chain reaction （Real-time PCR） and Western blot were applied to validate the expression of differential genes and related pathway proteins. Additionally， glucose （GLU） consumption， as well as lactate （LD） and adenosine triphosphate （ATP） content were assessed across all mouse groups.ResultsPharmacodynamic evaluation showed that， compared with the normal group， the model group exhibited significantly elevated serum levels of ALT， AST， TC， TG， and LDL-C （P<0.01）， significantly increased MDA level （P<0.01）， and significantly decreased GSH-Px level （P<0.05）. Compared with the model group， BBD intervention at different doses significantly reduced the serum levels of ALT， AST， TC， TG， and LDL-C （P<0.05， P<0.01）， increased GSH-Px level （P<0.05， P<0.01）， significantly decreased MDA level （P<0.01）， and ameliorated hepatic histopathological injury. Liver transcriptomic analysis revealed that， following high-dose BBD intervention， the core genes were mainly enriched in pathways related to inflammatory responses and energy metabolic reprogramming， including the interleukin-17 （IL-17） signaling pathway， the phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） signaling pathway， fructose and mannose metabolism， and glycolysis. Real-time PCR validation demonstrated that， compared with the normal group， the mRNA expression levels of glycolysis-related genes ［hexokinase 1 （HK1）， hexokinase 2 （HK2）， 6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 3 （PFKFB3）， 6-phosphofructo-2-kinase/fructose-2，6-bisphosphatase 4 （PFKFB4）， pyruvate kinase M （PKM）， and lactate dehydrogenase A （LDHA）］， as well as inflammatory cytokines ［tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， and interleukin-1β （IL-1β）］ were significantly upregulated in the model group （P<0.05， P<0.01）. Compared with the model group， the BBD-H group showed significantly decreased mRNA expression of HK1， HK2， PFKFB3， PFKFB4， PKM， LDHA， TNF-α， IL-6， and IL-1β （P<0.05， P<0.01）. Western blot results indicated that， compared with the normal group， the model group had significantly increased expression of glycolysis-related proteins ［glucose transporter 1 （GLUT1）， HK1， PFKFB3， and PKM］， inflammatory proteins ［interleukin-18 （IL-18）， TNF-α， and IL-1β］， and phosphorylated （p）-PI3K and p-Akt proteins （P<0.05， P<0.01）. Compared with the model group， the BBD-H group exhibited significantly decreased expression of GLUT1， HK1， PFKFB3， PKM， IL-18， TNF-α， IL-1β， p-PI3K， and p-Akt （P<0.05， P<0.01）. Metabolic indicator measurements showed that， compared with the model group， the BBD-H group showed significantly reduced GLU consumption， LD and ATP content （P<0.05， P<0.01）.ConclusionBBD may alleviate APAP-induced ALI through dual regulation of metabolic reprogramming and inflammatory responses， potentially via inhibition of the PI3K/Akt signaling pathway.关键词：Babaodan;acute liver injury;transcriptomics;metabolic reprogramming;inflammatory responses32|15|0更新时间：2026-09-16
- 摘要：ObjectiveTo explore the therapeutic effect and mechanism of Huangqi Xiayuxue decoction against hepatocellular carcinoma based on network pharmacology， animal experiments， and cell experiments.MethodsThe active ingredients and corresponding targets of Huangqi Xiayuxue decoction were screened via databases including the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP） and Bioinformatics Analysis Tool for Molecular Mechanism of Traditional Chinese Medicine （BATMAN-TCM）. Hepatocellular carcinoma-related targets were retrieved from the GeneCards database. The common targets shared by Huangqi Xiayuxue decoction and hepatocellular carcinoma were subjected to Gene Ontology （GO） functional annotation and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analyses. Huangqi Xiayuxue decoction-containing plasma was prepared. The cell counting kit-8 （CCK-8） assay was adopted to observe the effects of different volume fractions （5%， 10%， 15%， and 20%） of Huangqi Xiayuxue decoction-containing plasma on the proliferation of HepG2， MHCC-97H， Hepa1-6， and Huh-7 cells， and the concentration for subsequent experiments was determined. Flow cytometry was adopted to detect the effects of Huangqi Xiayuxue decoction-containing plasma （5%， 10%， 15%， and 20%） on the apoptosis of MHCC-97H cells. A mouse model of subcutaneous xenograft hepatocellular carcinoma was established. The model mice were assigned into low-， medium-， and high-dose （4.63， 9.25， 18.5 g·kg-1） Huangqi Xiayuxue decoction and sorafenib （20 mg·kg-1） groups. Body mass and tumor volume of mice were dynamically monitored during the intervention period. After 3 weeks of intervention， hematoxylin-eosin （HE） staining was performed to observe tumor morphology. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling （TUNEL） assay was employed to detect cell apoptosis. Immunohistochemistry （IHC） was adopted to examine the expression of cysteinyl aspartate-specific proteinase-3 （Caspase-3）， B-cell lymphoma-2 （Bcl-2）， and Bcl-2-associated X protein （Bax） in the tumor tissue. Real-time PCR and Western blot were employed to verify the changes in apoptosis-related factors and the phosphatidylinositol 3-kinase/protein kinase B/forkhead box O1 （PI3K/Akt/FoxO1） signaling pathway.ResultsA total of 220 common targets shared by Huangqi Xiayuxue decoction and hepatocellular carcinoma were screened out by network pharmacology， among which tumor protein p53 （TP53）， Akt1， and signal transducer and activator of transcription 3 （STAT3） were the core targets. Pathway enrichment analysis indicated that the common targets were involved in cell apoptosis and proliferation， as well as the PI3K/Akt and FoxO signaling pathways. Cell experiments showed that compared with the blank plasma group， all volume fractions of Huangqi Xiayuxue decoction-containing plasma inhibited the proliferation of HepG2， MHCC-97H， Hepa1-6， and Huh-7 cells （P<0.01）. The proportion of early apoptotic cells in MHCC-97H cells was increased after treatment with different volume fractions of Huangqi Xiayuxue decoction-containing plasma （P<0.01）. Animal experiments revealed that Huangqi Xiayuxue decoction inhibited the growth of tumor volume， promoted tumor cell apoptosis in the high-dose group， up-regulated the protein and mRNA levels of Bax and Caspase-3， down-regulated the protein and mRNA levels of Bcl-2， and reduced the phosphorylation level of the PI3K/Akt/FoxO1 signaling pathway （P<0.05， P<0.01）.ConclusionHuangqi Xiayuxue decoction exerts anti-hepatocellular carcinoma effects by inhibiting the activation of the PI3K/Akt/FoxO1 signaling pathway and promoting hepatocellular carcinoma cell apoptosis.关键词：hepatocellular carcinoma;network pharmacology;Huangqi Xiaoyuxue decoction;apoptosis;phosphatidylinositol 3-kinase/protein kinase B/forkhead box O（PI3K/Akt/FoxO） signaling pathway;replenishing Qi and activating blood18|7|0更新时间：2026-09-16
- 摘要：ObjectiveTo validate the therapeutic effect of Yinqi Sanhuang Jiedu decoction （YQSH） on a mouse model of carbon tetrachloride （CCl4）-induced liver fibrosis and to investigate its correlations with the Piezo-type mechanosensitive ion channel component 1 （Piezo1）-Yes-associated protein （YAP） mechanical signaling axis and macrophage polarization.MethodsFifty-four C57BL/6J mice were randomized into a blank control group， a 4-week model group， a 6-week model group， a 8-week model group， a positive drug （silymarin， 55 mg·kg-1·d-1） group， and low-， medium-， and high-dose （8.325， 16.65， 33.3 g·kg-1·d-1， respectively） YQSH groups. Except the 6-week model group （n=12）， each of the other groups had 6 mice. Mice in other groups except the blank control group received intraperitoneal injections of 10% CCl4 twice weekly for the modeling of liver fibrosis. Drug interventions began one week after the initial modeling through gavage， and the blank control and model groups received 0.2 mL of normal saline via gavage. The histopathological changes and collagen deposition in the liver were observed via hematoxylin-eosin （HE）， Masson's trichrome， and Sirius red staining. Serum activities of alanine aminotransferase （ALT） and aspartate aminotransferase （AST）， as well as serum levels of total protein （TP）， albumin （ALB）， total bilirubin （TBIL）， hyaluronic acid （HA）， laminin （LN）， procollagen type Ⅲ （PCⅢ）， and collagen type Ⅳ （Ⅳ-C）， were measured. The levels of tumor necrosis factor-α （TNF-α） and interleukin-1β （IL-1β） in the liver tissue were determined by enzyme-linked immunosorbent assay （ELISA）. The protein and mRNA levels of Piezo1 and YAP1 in the liver tissue were determined by immunohistochemistry （IHC） and Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）， respectively. Co-localization of Piezo1 with YAP1， and YAP1 with inducible nitric oxide synthase （iNOS） was observed by the immunofluorescence （IF） assay. The proportions of M1-type （F4/80+CD80+） and M2-type （F4/80+CD206+） macrophages in the liver tissue were examined by flow cytometry. Gene Ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） enrichment analyses and gene set enrichment analysis （GSEA） were performed through transcriptomic sequencing.ResultsCompared with the blank control group， the model group exhibited gradually worsened liver fibrosis at the 4th， 6th， and 8th weeks. The 6- and 8-week model groups showcased inflammatory cell infiltration and collagen deposition in the liver （P<0.01） and upregulated protein levels of both Piezo1 and YAP1 （P<0.01）. Compared with the model groups， treatment with YQSH improved the liver function （P<0.05， P<0.01）， alleviated liver fibrosis （P<0.05， P<0.01）， and reduced intrahepatic inflammatory cell infiltration and collagen deposition （P<0.01）. Furthermore， the treatment downregulated the protein and mRNA levels of Piezo1 and YAP1 （P<0.05， P<0.01）， lowered the levels of inflammatory factors TNF-α and IL-1β （P<0.05， P<0.01）， and decreased the ratio of CD80 （M1-type）/CD206 （M2-type） macrophage proteins （P<0.01）. The IF assay showed co-localization of YAP1 with Piezo1 and iNOS. Compared with the model groups， YQSH treatment downregulated the expression of Piezo1， YAP1， and iNOS （P<0.05， P<0.01）. Transcriptomic analysis suggested that the anti-liver fibrosis effect of YQSH may be related to the Hippo signaling pathway （P<0.05）.ConclusionThe anti-liver fibrosis effect of YQSH may be related to its inhibition of the Piezo1-YAP signaling axis and regulation of macrophage polarization.关键词：liver fibrosis;Yinqi Sanhuang Jiedu decoction;Piezo-type mechanosensitive ion channel component 1 （Piezo1）;Yes-associated protein 1 （YAP1）;macrophage polarization40|10|0更新时间：2026-09-16
- 摘要：ObjectiveTo observe the effect of modified Huanglian Wendantang on oxidative stress in metabolic syndrome.MethodsA total of 180 patients with metabolic syndrome treated in the outpatient clinics and wards of the First Affiliated Hospital of Heilongjiang University of Traditional Chinese Medicine from October 2023 to May 2025 were enrolled in this study. According to the randomized numerical table method， the patients were assigned into two groups （90 cases）. The basic treatment of the two groups was the same， and the observation group was additionally treated with modified Huanglian Wendantang. The course of treatment was 3 months. The two groups were compared in terms of traditional Chinese medicine （TCM） efficacy， obesity degree ［waist circumference （WC）， body mass index （BMI）， waist-to-hip ratio （WHR）， waist-to-height ratio （WHtR）］， blood pressure indicators ［systolic blood pressure （SBP） and diastolic blood pressure （DBP）］， lipids and glucose indicators ［total cholesterol （TC）， triglycerides （TG）， high-density lipoprotein cholesterol （HDL-C）， low-density lipoprotein cholesterol （LDL-C）， fasting insulin （FINS）， fasting glucose （FPG）， 2-hour postprandial glucose （2 h PG）， and glycosylated hemoglobin （HbA1c）］， insulin resistance indicators ［homeostatic model assessment for insulin resistance （HOMA-IR）， triglyceride-glucose index （TYG index）， triacylglycerol-to-high-density lipoprotein cholesterol （TG/HDL） ratio］， oxidative stress indicators ［malondialdehyde （MDA）， superoxide dismutase （SOD）， glutathione （GSH）， glutathione peroxidase （GSH-Px）， catalase （CAT）， and reactive oxygen species （ROS）］， and the safety of treatment.ResultsIn terms of TCM efficacy， the treatment in the observation group was significantly effective in 46 cases， effective in 30 cases， and ineffective in 10 cases， with the total effective rate of 88.4%. The treatment in the control group was significantly effective in 33 cases， effective in 28 cases， and ineffective in 23 cases， with the total effective rate of 72.6%. The observation group had higher total effective rate than the control group （χ2=11.26，P<0.05）. After treatment， both groups showed declined levels of WC， BMI， WHR， WHtR， SBP， DBP， TC， TG， LDL-C， FPG， FINS， 2 h PG， HbA1c， HOMA-IR， TG/HDL ratio， TYG index， MDA， and ROS and elevated levels of HDL-C， SOD， GSH， GSH-Px， and CAT （P<0.05）. After treatment， the observation group showed lower levels of WC， BMI， WHR， WHtR， TC， TG， LDL-C， FPG， FINS， 2 h PG， HbA1c， HOMA-IR， TG/HDL ratio， TYG index， MDA， and ROS and higher levels of HDL-C， SOD， GSH， GSH-Px， and CAT than the control group （P<0.05）. However， after treatment， there was no significant difference in SBP or DBP between the observation group and the control group. No significant adverse reactions were observed in either group.ConclusionModified Huanglian Wendantang can significantly alleviate metabolic syndrome symptoms and reduce oxidative stress， exhibiting antioxidant effects. Moreover， it does not induce adverse reactions， demonstrating safety.关键词：metabolic syndrome;modified Huanglian Wendantang;oxidative stress32|12|0更新时间：2026-09-16
- 摘要：ObjectiveTo evaluate the effects of Qingre Huoxue prescription combined with methotrexate （MTX） and folic acid （FA） on homocysteine （Hcy） levels and disease activity in patients with rheumatoid arthritis （RA） complicated by hyperhomocysteinemia （HHcy）.MethodsOn the basis of a multicenter real-world cohort from the China Registry of Traditional Chinese Medicine for Rheumatism （CERTAIN） platform，408 patients with RA complicated by HHcy were selected and included in this study. Treatment with Qingre Huoxue prescription was used as the exposure factor. According to whether Qingre Huoxue prescription was combined with MTX and FA，patients were assigned into an exposure group of 281 cases and a control group of 127 cases. Follow-ups were conducted every three months，with the primary outcome indicator being the achievement rate of target Hcy level. A generalized estimating equation model was adopted to analyze the dynamic changes in Hcy level under different medication regimens. Kaplan-Meier analysis was performed to evaluate the cumulative achievement rate of target Hcy level in the two groups，and Cox regression analysis was conducted to explore the predictive factors affecting the achievement rate of target Hcy level. Changes in erythrocyte sedimentation rate （ESR），C-reactive protein （CRP），28-joint disease activity score （DAS 28），and Health Assessment Questionnaire-Disability Index （HAQ-DI） scores before and after the first combined treatment with Qingre Huoxue prescription were compared between the two groups.ResultsThe Hcy level in the exposure group showed a gradual decreasing trend over time，while the decrease in Hcy level was not significant in the control group. At the 12-month follow-up，the achievement rate of target Hcy level in the exposure group （124/281，44.13%） was higher than that in the control group （23/127，18.11%，P<0.01）. Multivariable Cox regression analysis showed that treatment with Qingre Huoxue prescription ［hazard ratio（HR）=3.013，95% confidence interval （CI） 2.188-4.149， P<0.001］， absence of comorbidities （HR=2.035， 95%CI 1.352-3.061， P<0.001）， and baseline Hcy <15 μmol·L-1 （HR=1.810， 95%CI 1.390-2.357， P<0.001） were significantly associated with an increased likelihood of achieving target Hcy levels within 6 months. In contrast， higher PGA scores were associated with a reduced likelihood of achieving target Hcy levels （HR=0.991， 95% CI 0.986-0.997， P=0.003）. After treatment，the exposure group demonstrated reductions in ESR，CRP，and DAS 28 scores （P<0.05） and had lower ESR，CRP and DAS 28 scores than the control group （P<0.05）.ConclusionEven after taking FA supplements，some RA patients undergoing MTX treatment still have high Hcy levels. When being used in conjunction with MTX and FA，Qingre Huoxue prescription can effectively lower the Hcy level and disease activity in RA patients with HHcy，outperforming Western treatment alone.关键词：rheumatoid arthritis;hyperhomocysteinemia;Qingre Huoxue prescription;achievement rate of target homocysteine level;real-world cohort study35|12|0更新时间：2026-09-16
- 摘要：ObjectiveTo observe the clinical efficacy and safety of Zhinao capsules in the treatment of mild and moderate sleep disorders in Alzheimer's disease patients with the syndrome of spleen-kidney deficiency and combined phlegm and stasis.MethodsA randomized， double-blind， placebo， controlled clinical trial design was adopted， and 60 Alzheimer's disease patients aged 50-85 years with mild and moderate sleep disorders due to spleen-kidney deficiency and combined phlegm and stasis were included. According to the randomized numble table method， the patients were assigned into a treatment group and a control group （30 in each group， with 29 patients in the treatment group and 28 patients in the control group finally completing the trial）. The treatment group was treated with donepezil hydrochloride tablets combined with Zhinao capsules， and the control group was treated with donepezil hydrochloride tablets combined with the simulant of Zhinao capsules for 12 weeks. The Pittsburgh sleep quality index （PSQI）， smart bracelet sleep monitoring， epworth sleeping scale （ESS）， Mini-Mental State Examination （MMSE）， Activities of Daily Living （ADL）， and traditional Chinese medicine symptoms were scored. Furthermore， the brain-derived neurotrophic factor （BDNF） and gamma-aminobutyric acid （GABA） levels were measured.ResultsAfter 12 weeks of treatment， the total response rate of clinical efficacy assessment in the treatment group reached 89.7%， which was significantly higher than that （21.4%） in the control group （Z=-5.14， P<0.01）. After treatment， the TCM symptom scores declined in both groups （P<0.01）， and the scores in the treatment group were lower than those in the control group （P<0.01）. After treatment， the treatment group showed decreased total score and seven component scores of the PSQI scale （P<0.05， P<0.01）， and the scores in the treatment group were lower than those in the control group （P<0.05， P<0.01）. After treatment， the treatment group showed increases in the duration of deep sleep， light sleep， rapid eye movement sleep， and total sleep at night and decreases in the time to fall asleep， the number of awakenings from sleep at night， and the time for sporadic daytime naps （P<0.01）. The control group did not show significant changes in the duration of light sleep， time to fall asleep， and number of awakenings from sleep at night. Moreover， the treatment group outperformed the control group in terms of the indicators above （P<0.05， P<0.01）. After treatment， the treatment group showed decreased scores of ESS， ADL and its subscales physical self-maintenance scale （PSMS）， and Instrumental Activities of daily living scale （IADLs） and increased score of MMSE and levels of BDNF and GABA （P<0.05， P<0.01）. There was no significant difference in PSMS between the two groups， and the treatment group was significantly better than the control group in terms of the rest of the above indicators （P<0.05， P<0.01）. Patients in neither groups complained of uncomfortable symptoms.ConclusionZhinao capsules have significant clinical efficacy in treating patients with mild and moderate sleep disorders in Alzheimer's disease patients with the syndrome of spleen-kidney deficiency and combined phlegm and stasis. Zhinao capsules can significantly reduce PSQI， ESS， and ADL scores， increase the MMSE score and the expression of BDNF and GABA， effectively optimize the structure of sleep， improve the intelligence， and enhance the ability of daily life， without causing uncomfortable symptoms. The mechanism may be related to the increase in the expression of sleep/wake-related neurotransmitters.关键词：mild and moderate sleep disorders in Alzheimer's disease;syndrome of spleen-kidney deficiency and combined phlegm and stasis;Zhinao capsules39|11|0更新时间：2026-09-16
- 摘要：ObjectiveTo evaluate the clinical efficacy and safety of Wenshen Yangxue decoction combined with endometrial microstimulation in the treatment of infertile patients with polycystic ovary syndrome （PCOS， syndrome of kidney-Yang deficiency and blood stasis）.MethodsA randomized， positive-drug parallel-controlled， open-label clinical study was conducted. A total of 240 infertile PCOS patients with the syndrome of kidney-Yang deficiency and blood stasis who met the inclusion and exclusion criteria were randomly assigned into 4 groups， with 60 patients in each group. The control group was treated with clomiphene citrate （50-100 mg·d-¹， orally for 5-10 consecutive days） for ovulation induction. On the basis of the therapy in the control group， the Wenshen group was additionally treated with Wenshen Yangxue decoction （250 mL， warm oral administration， twice daily， in the morning and evening）， and the stimulation group received endometrial microstimulation during the early follicular phase. The combined group was treated with clomiphene citrate plus Wenshen Yangxue decoction （at the same dosages as aforementioned） and endometrial microstimulation. The course of treatment for all the groups was 3 menstrual cycles. The pregnancy rate， ovulation status， sex hormone levels， glucose metabolism indicators， coagulation function， endometrial thickness， traditional Chinese medicine （TCM） symptom scores， and adverse reactions were observed in each group.ResultsA total of 239 patients were included in the final analysis， with 59 patients in the Wenshen group and 60 patients in each of the other three groups. The pregnancy rates were 43.3%（26/60） in the combined group and 32.2%（19/60） in the Wenshen group， both significantly higher than that （10%） in the control group （χ2=17.56，P<0.01）. Compared with the control group， the combined and Wenshen groups had increased mature follicle rates （P<0.01）， while the Wenshen group showed a decreased luteinization rate （P<0.05）. All the groups exhibited significant reductions in TCM symptom scores after treatment， and the Wenshen and combined groups had lower scores than the control group （P<0.01）. No statistically significant difference was found in the incidence of adverse events among the four groups， and all the adverse events were mild.ConclusionWenshen Yangxue decoction combined with endometrial microstimulation can alleviate the TCM symptoms of infertile PCOS patients with the syndrome of kidney-Yang deficiency and blood stasis， promote follicular maturation and ovulation， increase the cumulative pregnancy rate， and has good safety. It can provide new clinical evidence for the integrated traditional Chinese and Western medicine treatment of PCOS infertility.关键词：Wenshen Yangxue decoction;endometrial microstimulation;polycystic ovary syndrome;infertility;syndrome of kidney-Yang deficiency and blood stasis1|0|0更新时间：2026-09-16
- 摘要：ObjectiveTo construct a risk prediction model for chronic atrophic gastritis （CAG） that combines disease and syndrome by integrating spleen deficiency and blood stasis syndrome scores， gastric stem cell marker analysis， and network pharmacology and to elucidate the mechanism link between spleen deficiency， blood stasis， and gastric stem cell dysregulation.MethodsA total of 60 patients were stratified into high-risk CAG， low-risk CAG， and non-atrophic groups based on the operative link for gastritis assessment （OLGA）/operative link for gastric intestinal metaplasia assessment （OLGIM） stages. General data and syndrome scores of the patients were collected. Immunohistochemistry was employed to measure the protein levels of leucine-rich repeat-containing G protein-coupled receptor 5 （LGR5）， trefoil factor 2 （TFF2）， and β-catenin in gastric mucosa across groups. Transcriptomic data （GSE130823） from the Gene Expression Omnibus （GEO） database were analyzed to validate the expression of these molecular markers at the gene level. A Firth penalized maximum likelihood logistic regression model was employed to integrate clinical， molecular， and TCM syndrome data to develop a CAG risk prediction model. Finally， network pharmacology analysis was conducted on spleen-invigorating herbs （Astragali Radix， Atractylodis Macrocephalae Rhizoma， and Dioscorea Rhizoma） and blood-activating herbs （Hedyotis diffusa， Salviae Miltiorrhizae Radix et Rhizoma， and Curcumae Rhizoma） to identify overlapping targets between these herbs and differentially expressed genes between low-grade intraepithelial neoplasia （LGIN） and gastritis， thereby clarifying the role of spleen deficiency and blood stasis in CAG progression from a pharmacological perspective.ResultsHigh-risk CAG patients exhibited higher blood stasis scores （4.60±1.50，2.62±1.32， P<0.01）， progressive nuclear accumulation of β-catenin （A 0.28-0.53， P<0.01）， and an increased LGR5+/TFF2+ ratio （A 1.02-1.92， P<0.01）. Blood stasis scores were correlated with LGR5/TFF2 imbalance （P=0.03） and activation of the Wnt/β-catenin signaling pathway （CTNNB1 increase， log2=0.78）. The integrated prediction model （blood stasis score≥5 + β-catenin>0.38 + LGR5/TFF2>1.5） outperformed a pure biomarker approach ［Area Under the Curve （AUC） 0.92，0.89， ΔAUC=0.03， P=0.02］. Moreover， network pharmacology revealed 66 overlapping targets between spleen-invigorating/blood-activating herbs and LGIN， which were functionally enriched in mucosal repair and anti-oxidative stress， and negatively correlated with the Wnt/β-catenin signaling pathway （P<0.01）.ConclusionThis study developed an integrated risk prediction model for CAG by combining TCM spleen deficiency and blood stasis syndromes with gastric stem cell molecular markers. Furthermore， it proposed for the first time the "blood stasis-Wnt/β-catenin-stem cell axis" hypothesis， preliminarily elucidating that spleen deficiency and blood stasis may exacerbate gastric stem cell dysregulation and promote malignant transformation of CAG through hypoxia-induced Wnt activation. This provides a theoretical foundation and a translational tool for risk stratification and multi-target TCM intervention in CAG.关键词：chronic atrophic gastritis;risk prediction model;spleen deficiency syndrome;blood stasis syndrome;gastric stem cells1|0|0更新时间：2026-09-16
- 摘要：ObjectiveThis study aimed to investigate the mechanism by which Luoshi Neiyi prescription treats endometriosis （EMs） through regulating ferroptosis， and to screen key metabolites and analyze their association with ferroptosis.MethodsClinical samples of normal endometrium from patients without EMs and eutopic and ectopic endometrium from EMs patients （10 cases each） were collected and divided into control group， eutopic group， and EMs group. Hematoxylin-eosin （HE） staining was performed to observe ectopic lesions of EMs. Immunohistochemistry was used to detect the expression of solute carrier family 7 member 11 （SLC7A11） and glutathione peroxidase 4 （GPX4）. Enzyme-linked immunosorbent assay （ELISA） was adopted to determine the levels of malondialdehyde （MDA）， ferrous ion （Fe2+）， GPX4 and glutathione （GSH） in endometrial tissues， as well as serum levels of Fe2+， GPX4 and GSH. Real-time quantitative polymerase chain reaction （Real-time PCR） was used to detect the mRNA expression of SLC7A11， GPX4， transferrin receptor （TFR） and ferritin heavy chain 1 （FTH1）. In the in vitro experiment， primary stromal cells were isolated from ectopic lesions of EMs patients. Cell counting kit-8 （CCK-8） was used to determine the optimal concentration of drug-containing serum for intervention. The level of reactive oxygen species （ROS） was measured， and Real-time PCR was applied to detect ferroptosis-related indicators. In the animal experiments， an EM rat model was established， and the rats were randomly assigned to the sham operation group， EMs group， low-dose Luoshi Neiyi Formula group （7.87 g·kg-1）， high-dose Luoshi Neiyi prescription group （15.74 g·kg-1）， and danazol group （42 mg·kg-1）. Untargeted metabolomics detection and pathway enrichment analysis were conducted on serum samples from patients and rats. Spearman correlation analysis was performed to assess the relationship between differential metabolites and ferroptosis indicators. The correlations between differential metabolites in patient endometrium and serum and key ferroptosis indicators （GPX4， Fe2+， MDA， GSH） as well as ferroptosis-related mRNAs （GPX4， SLC7A11， FTH1） were analyzed， and correlation heatmaps were generated accordingly.ResultsCompared with normal eutopic endometrium， ectopic lesions in EMs patients showed glandular disorganization and stromal fibrosis. In ectopic endometrium， the contents of MDA， ROS， and Fe2+ decreased， while GPX4 level increased， and the mRNA expression of SLC7A11 and GPX4 was upregulated （P<0.05， P<0.01）. In serum， the levels of GPX4 and Fe2+ were elevated， whereas the GSH level declined， suggesting abnormalities in ferroptosis-related pathways in ectopic lesions （P<0.05， P<0.01）. After intervention with Luoshi Neiyi prescription-containing serum， the intracellular ROS level in ectopic endometrial stromal cells was elevated， the mRNA expression of SLC7A11 and GPX4 was downregulated， and TFR mRNA expression was upregulated （P<0.05， P<0.01）. Metabolomics analysis revealed 1104 and 198 differential metabolites in EMs patients and EMs rats， respectively， compared with their corresponding control groups， and both low-dose and high-dose Luoshi Neiyi prescription were found to regulate this metabolic disturbance， with the core regulatory pathways mainly involving arginine and proline metabolism. Correlation analysis showed that the glycerophospholipids including PI（16∶0/17∶0） and PI［18∶2（9Z，12Z）］ were negatively correlated with GPX4 and positively correlated with MDA， while 17α-hydroxyprogesterone was positively correlated with GPX4， SLC7A11， and FTH1 q<0.05）.ConclusionLuoshi Neiyi prescription may systematically ameliorate disease-associated metabolic dysregulation via modulation of the serum arginine and proline metabolism pathway， and may regulate ferroptosis in ectopic lesions through a mechanism potentially linked to the serum glycerophospholipid and steroid metabolism pathways. Collectively， these findings provide experimental evidence for the clinical application of Luoshi Neiyi prescription.关键词：Luoshi Neiyi prescription;endometriosis;animal experiment;ferroptosis;serum metabolism15|10|0更新时间：2026-09-16
- 摘要：Cardiac aging is a key factor in the onset and progression of cardiovascular diseases. Investigating the traditional Chinese medicine （TCM） pathogenesis and therapeutic principles of cardiac aging is of great importance for curbing the common phenomenon of the heart aging faster than the body and implementing the national strategy in response to population aging. Essence （Jing）， Qi， and spirit （Shen） are the origin， driving force， and manifestation of life， respectively. The Essence-Qi-spirit theory within the Qi-collateral doctrine delineates the core pathogenesis and therapeutic principles of aging. This framework identifies kidney essence deficiency as the fundamental cause of aging， with primordial Qi depletion as a key factor and the consumption of body and spirit as its manifestations. Corresponding treatment principles involve tonifying the kidney to replenish essence， warming and supporting primordial Qi， and nourishing the body and spirit. During the process of tonifying the kidney， regulating Yin and Yang remains essential. Relevant studies indicate that this theoretical system provides significant guidance for anti-aging research in TCM. Guided by the Essence-Qi-spirit theory within the Qi-collateral doctrine， this paper posits that kidney essence constitutes the material foundation for cardiac development， and primordial Qi acts as the fundamental driver of cardiac function. Physical form and spirit together provide the structural carrier and functional manifestation of the heart. We further propose the core pathogenesis and therapeutic principles for cardiac aging. The fundamental pathogenesis lies in the deficiency and decline of kidney essence， leading to malnourishment of the heart. The key pathogenesis is the deficiency of primordial Qi， resulting in obstruction of the heart collateral. The manifestation involves the accumulation in the collateral and the dysfunction of the heart spirit. The corresponding treatment principles are tonifying the kidney and replenishing essence to nourish the heart， warming and reinforcing primordial Qi to unblock the heart collateral， and fortifying the physical form to invigorate the spirit mechanism. Existing studies demonstrate that Bazi Bushen Capsules， with the effects of tonifying the kidney， replenishing essence， warming primordial Qi， and fortifying the physical form and spirit， can delay cardiac aging. Guided by the Essence-Qi-spirit theory within the Qi-collateral doctrine， these findings support the development of effective herbal formulas to intervene in cardiac aging.关键词：Qi-collateral doctrine;essence-Qi-spirit theory;Bazi Bushen capsules;cardiac aging31|13|0更新时间：2026-09-16
- 摘要：Metabolic syndrome （MS） is a clinical syndrome characterized by obesity， insulin resistance， and dyslipidemia， and chronic inflammation is closely associated with its pathogenesis. The imbalance between pro-inflammatory and anti-inflammatory macrophage polarization， as one of the core pathological mechanisms of chronic inflammation， is a crucial driver of MS progression. According to Essential Questions in Yellow Emperor's Inner Canon： Distinctive Theory on Meridians and Diseased Pulses， "the spleen Qi dispersing essence... along all the meridians and collaterals". When the spleen fails in transportation and transformation， the distribution of refined essence becomes disordered， leading to internal accumulation of phlegm-dampness， forming a dynamic pathological state of "root deficiency with branch excess". Accordingly， the core traditional Chinese medicine （TCM） pathogenesis of MS is closely related to "spleen failing in transportation and transformation coupled with the internal accumulation of phlegm-dampness"； however， its modern biological basis remains elusive. Therefore， based on the theory of "spleen Qi dispersing essence" and recent advances in immunometabolism， this paper explored the modern scientific connotation of the TCM pathogenesis of MS from the perspective of macrophage polarization driven by glucose metabolic reprogramming. Through theoretical analysis and literature integration， it was proposed that mitochondrial oxidative phosphorylation participates in the energy metabolism process of "spleen Qi dispersing essence". The dysfunction of the spleen's transportation and transformation prompts macrophage metabolism to shift toward glycolysis， resulting in the accumulation of lactate and succinate， which represents the microscopic manifestation of "refined essence deviating from proper transformation" and can be defined as "microscopic phlegm-dampness". These metabolites subsequently drive M1 macrophage polarization via the hypoxia-inducible factor-1α （HIF-1α）/nuclear factor-κB （NF-κB） signaling pathway， triggering the release of pro-inflammatory cytokines and inducing systemic chronic low-grade inflammation， ultimately manifesting as insulin resistance， lipid metabolic disorders， and other core components of MS， thus achieving immune amplification from local "microscopic phlegm-dampness" to systemic "internal accumulation of phlegm-dampness". Therefore， macrophage polarization driven by glucose metabolic reprogramming constitutes an important biological link connecting the TCM concept of "spleen failing to disperse essence" with the pathology of MS. Furthermore， this paper reviewed the potential mechanisms by which TCM herbal formulas and their monomeric components that "restore spleen transportation and resolve phlegm-dampness" ameliorate MS by modulating macrophage metabolic remodeling， thereby providing novel biological connotations for the modern interpretation of the theory of "spleen Qi dispersing essence". Future research should integrate multi-omics technologies with disease-syndrome animal models to elucidate the regulatory network of formulas that "restore spleen transportation and resolve phlegm-dampness". Additionally， the feasibility of utilizing macrophage metabolic phenotypes as objective diagnostic biomarkers for the phlegm-dampness syndrome in MS warrants further investigation.关键词：metabolic syndrome;phlegm-dampness;spleen Qi dispersing essence;macrophages;metabolic reprogramming21|4|0更新时间：2026-09-16
- 摘要：Primary osteoporosis （POP） is a metabolic bone disease characterized by reduced bone mass， degenerated bone microstructure， and increased bone fragility. Its pathogenesis involves the interaction of multiple factors such as genetics， aging， endocrine， and environment， which remain incompletely elucidated. Mitochondrial dysfunction can lead to insufficient adenosine triphosphate （ATP） production and abnormal accumulation of reactive oxygen species （ROS）， activating oxidative stress and inflammation pathways， thereby inhibiting osteoblast differentiation and promoting osteoclast activation， exacerbating the negative bone metabolism balance in POP. Mitochondrial autophagy， as the core mechanism of mitochondrial quality control， selectively identifies and clears damaged mitochondria to effectively reduce ROS accumulation and energy metabolism disorders， thus maintaining the balance between osteoblast and osteoclast differentiation. It plays a critical role in maintaining bone homeostasis and the prevention and treatment of POP. The traditional Chinese medicine （TCM） theory of Qi transformation shares similarities with the functions of mitochondria in energy generation and substance conversion. The pathological state of Qi deficiency and stagnation may be associated with mitochondrial autophagy dysfunction， and the pathogenic characteristics of combined phlegm and stasis align with the metabolic waste accumulation induced by obstructed autophagy flow. This article explores the correlation of the theory of Qi deficiency and stagnation with mitochondrial autophagy and elucidates its potential role in the pathogenesis of POP. Additionally， considering the pathogenesis features of POP， which involve deficiency causing stagnation and a mixture of deficiency and excess， this article proposes a novel therapeutic approach： tonifying Qi to support the body and unblocking collaterals to resolve stagnation from the perspective of mitochondrial autophagy. This article aims to provide theoretical support and research insights for further exploration of TCM in the prevention and treatment of POP.关键词：primary osteoporosis;Qi deficiency and stagnation;mitochondrial autophagy;bone metabolism;traditional Chinese medicine1|0|0更新时间：2026-09-16
- 摘要：ObjectiveTo construct a risk prediction model for carotid artery plaques in high-risk populations of stroke based on five machine learning methods.MethodsThe clinical information of the high-risk population of stroke was collected. Factor analysis and statistical analysis of syndrome elements were conducted on their traditional Chinese medicine （TCM） symptoms and tongue and pulse manifestations. On the basis of the results of factor analysis and variable screening， five machine learning methods-classification and regression tree （CART） decision tree， support vector machine （SVM）， back propagation（BP） neural network， logistic regression， and random forest-were used to construct the risk prediction model for carotid artery plaques.ResultsThe most common TCM syndrome elements in the high-risk population of stroke was Qi deficiency. The scores of Qi deficiency， Yin deficiency， and Yang deficiency in the population with carotid artery plaques were higher than those without carotid artery plaques （P<0.05）. The CART decision tree， SVM， logistic regression， BP neural network， and random forest models showed the areas under the receiver operating characteristic （ROC） curves of 0.71， 0.75， 0.76， 0.76， and 0.75， the accuracy rates of 68.94%， 69.27%， 69.44%， 70.10%， and 69.60%， the precision rates of 68.56%， 68.53%， 68.75%， 69.74%， and 69.42%， the recall rates of 68.91%， 67.93%， 67.92%， 68.10%， and 67.31%， and the F1 values of 0.69， 0.68， 0.68， 0.68， and 0.68， respectively.ConclusionAmong the high-risk population of stroke， the most frequently distributed TCM syndrome element is Qi deficiency， with the rest mainly being fire heat， Yin deficiency， Yang deficiency， phlegm dampness， blood stasis， and Qi stagnation. Deficiency syndrome may be a major factor leading to carotid artery plaques in the high-risk population of stroke. The BP neural network model demonstrates better performance in predicting the risk of carotid artery plaques in the high-risk population of stroke. People with carotid artery plaques are more likely to present with symptoms such as a heavy head， dizziness， headache， and thready pulse. The primary community benefits more widely when the BP neural network model is adopted to predict the risk of carotid artery plaques in the high-risk population of stroke over 40 years old.关键词：carotid artery plaque;prediction model;traditional Chinese medicine syndrome element;stroke1|0|0更新时间：2026-09-16
- 摘要：The nose-to-brain pathway refers to a significant drug delivery route through which substances traverse the unique anatomical structures of the nasal cavity to directly access the central nervous system， bypassing the blood-brain barrier. Its core advantage lies in utilizing the olfactory and trigeminal nerves， enabling peripheral drug administration to rapidly and efficiently reach the brain， thereby avoiding the drug loss and bioavailability reduction associated with oral or intravenous routes due to the circulatory system and blood-brain barrier limitations. In recent years， with in-depth research into the neuroanatomy of the olfactory system， nasal mucosal barrier properties， and neural regulatory mechanisms， the potential application of the nose-to-brain pathway in neurological diseases has attracted increasing attention. Traditional Chinese medicine （TCM） essential oils， characterized by strong lipophilicity， small molecular weights， volatility， and diverse chemical components， are highly compatible with the physiological characteristics of the nose-to-brain pathway， thus serving as promising carriers for brain-targeted drug delivery， enhancing drug bioavailability， and exerting neuroprotective effects. On this basis， this review systematically summarizes the anatomical and physiological bases for the delivery of TCM essential oils via the nose-to-brain pathway， the patterns of drug transport and brain distribution， clinical and animal study examples in neurological diseases， the associated molecular mechanisms and signaling pathways， and the progress in the development of novel nasal essential oil formulations. Additionally， the review analyzes the current challenges in this field and proposes strategies for future research and application. By systematically discussing the nose-to-brain pathway and the delivery mechanisms of TCM essential oils， this study aims to provide theoretical support for drug development， mechanism exploration， and formulation innovation in the treatment of neurological diseases， while also offering scientific guidance for further research and clinical applications of the nose-to-brain delivery system.关键词：essential oils;nose-to-brain pathway;drug delivery;neurological disease;signaling pathway42|9|0更新时间：2026-09-16
- 摘要：Diabetic kidney disease （DKD）， a prevalent microvascular complication of diabetes mellitus， is characterized by intricate pathophysiological mechanisms and persistent clinical management challenges. Historically， glomerular injury has been regarded as the central pathological hallmark of DKD， with research predominantly focusing on hyperfiltration， glomerular basement membrane thickening， and podocyte dysfunction. Emerging evidence， however， underscores the renal tubule-not merely as a passive bystander but as an early initiator and pivotal driver-in DKD pathogenesis. Hyperglycemia， metabolic dysregulation， and chronic low-grade inflammation induce tubular epithelial cell injury at early disease stages. Such injury disrupts tubuloglomerular feedback， thereby elevating intraglomerular pressure and sustaining hyperfiltration. Concurrently， injured tubular cells secrete pro-inflammatory cytokines and profibrotic factors， promoting epithelia-mesenchymal transition， interstitial hypoxia， and progressive tubulointerstitial fibrosis that ultimately culminate in irreversible decline of renal function. This "tubule-first" paradigm represents a fundamental shift from the classical glomerulocentric model and redefines the conceptual framework of DKD progression. Traditional Chinese medicine（TCM）， with its inherent advantages of multi-component synergy， multi-target engagement， and systemic homeostatic regulation， has demonstrated compelling renoprotective effect， particularly in preserving tubular integrity and function， mitigating tubular cellular stress， and indirectly alleviating glomerular hemodynamic burden. Accumulating preclinical and clinical evidence supports the efficacy of numerous single herbs and standardized formulae of TCM in attenuating tubulointerstitial injury and slowing down DKD progression. This review systematically delineates the sequential pathogenic cascade-from initial tubular insult to secondary glomerular deterioration-and critically evaluates the mechanism basis and translational potential of TCM-based interventions targeting tubular resilience. We aim to provide a refined pathophysiological rationale and actionable insights for optimizing clinical strategies and accelerating the development of novel therapeutics for DKD.关键词：diabetic kidney disease;renal tubule;glomerulus;tubuloglomerular feedback;traditional Chinese medicine39|12|0更新时间：2026-09-16
- 摘要：Chronic heart failure （CHF）， as the terminal stage of various cardiovascular diseases， is characterized by a prolonged course and a high mortality rate， posing a serious threat to human health and life. According to physician Sun Yikui's theory of "Mingmen Dongqi" （dynamic Qi of life gate） in the Ming Dynasty and the modern medicine concept of mitochondrial quality control （MQC）， this paper systematically explores the pathogenic mechanisms and evolutionary patterns of CHF， as well as its intrinsic connection with microstructural homeostasis， and further proposes potential traditional Chinese medicine （TCM） intervention strategies. CHF is often caused by damage to the heart Qi at the early stage. As the disease progresses， prolonged illness affects the kidneys， leading to the dynamic Qi decline of life gate. Further， it results in the failure of the functions of sustaining and consolidating， causing the disintegration of the physical form， which corresponds to mitochondrial kinetic disorders. The deficiency in primary driving force results in impaired Qi transformation， corresponding to mitochondrial autophagy dysfunction， forming a pathological transmission chain of "life gate-mitochondrion" that ultimately leads to myocardial structural disintegration and energy metabolism failure. Modern research indicates that patients with CHF exhibit significant MQC imbalance. Disrupted mitochondrial dynamics lead to network fragmentation， and impaired autophagy causes metabolic blockage， constituting the key microscopic mechanisms underlying ventricular remodeling and pump failure. Chinese herbal medicines， such as those with the effects of warming and tonifying kidney Yang or reinforcing healthy Qi， can intervene in multiple signaling pathways-including PTEN-inducible kinase 1 （PINK1）/Parkin and AMP-activated protein kinase/dynamin-related protein 1 （AMPK/Drp1）-to regulate mitochondrial dynamics and autophagy activity. This repairs damaged MQC networks and improves the microenvironment of myocardial energy metabolism. These intervention strategies align closely with the TCM therapeutic principles of warming and tonifying life gate， replenishing Qi， and activating blood， demonstrating the advantages of holistic regulation based on kidney-centered treatment and mitochondrial-targeted approaches. By integrating the "Mingmen Dongqi" theory with the MQC mechanism， this paper establishes a theoretical framework for the integrated prevention and treatment of CHF， offering new perspectives and insights for clinical practice and future research.关键词：chronic heart failure;Mingmen DongQi;mitochondrial quality control;mitochondrial dynamics;mitochondrial autophagy1|0|0更新时间：2026-09-16
- 摘要：The co-occurrence of diabetes mellitus complicated with depression （DD） is a clinically prevalent comorbidity characterized by complex pathogenesis and challenging therapeutic management， severely impairing patients' quality of life. Recent research indicates that dysregulation in microglia-neuron interaction plays a pivotal role in the pathological progression of DD. Sustained hyperglycemia can activate central microglia， promoting the activation of NOD-like receptor protein 3（NLRP3） inflammasome and the release of abundant pro-inflammatory cytokines， such as interleukin-1β （IL-1β） and tumor necrosis factor-α （TNF-α）， which trigger neuroinflammation. This cascade leads to hippocampal neuronal damage， impaired synaptic plasticity， and neurotransmitter imbalances， ultimately exacerbating depressive-like behaviors. Traditional Chinese medicine （TCM） offers advantages in preventing and treating DD through its multi-component， multi-target， and holistic regulatory approach. TCM can intervene in excessive microglial activation and their aberrant interactions with neurons by modulating neurotrophic signaling pathways such as brain-derived neurotrophic factor （BDNF）/tyrosine receptor kinase B （TrkB）， suppressing neuroinflammation， preserving neuronal structure and function， regulating synaptic plasticity， and improving glucose and lipid metabolism， thereby exerting synergistic therapeutic effects. Focusing on the role of microglia-neuron interaction in the pathological progression of DD， this review systematically elaborates on the research progress of TCM in regulating this interactive process， providing new perspectives and potential targets for the clinical prevention and treatment of DD.关键词：diabetes mellitus complicated with depression;microglia;neuron;traditional Chinese medicine;mechanism25|15|0更新时间：2026-09-16
- 摘要：Diabetic microvascular complications （DMC） are major chronic complications of diabetes，primarily including diabetic kidney disease （DKD），diabetic retinopathy （DR），diabetic cardiomyopathy （DCM），and diabetic peripheral neuropathy （DPN）. These complications significantly impact patients' quality of life and prognosis. Modern medicine primarily focuses on symptomatic control in the treatment of DMC，with limited ability to reverse the disease progression. Endoplasmic reticulum stress （ERS），as a central event under hyperglycemic toxicity，is not only a key cause of pancreatic β-cell dysfunction （reduced insulin synthesis and secretion） but also a core driver of damage in various target organs of DMC. It activates three signaling pathways of the unfolded protein response （UPR）-inositol-requiring enzyme 1 （IRE1），activating transcription factor 6 （ATF6），and protein kinase R-like endoplasmic reticulum kinase （PERK），intertwining processes such as autophagy，apoptosis，oxidative stress，and calcium homeostasis imbalance. Traditional Chinese medicine （TCM） offers multi-target and multi-pathway therapeutic advantages and can curb the pathological progression of DMC by regulating ERS. This article systematically reviews the relationships of ERS with pancreatic β-cell function，insulin synthesis，and insulin secretion，and elucidates the core signaling pathways through which ERS mediates DMC. Furthermore，it categorizes and summarizes experimental evidence and mechanisms of single medicinal herbs and their extracts，TCM compound formulas，and modern TCM preparations in regulating ERS for the treatment of various DMC subtypes. Finally，this article proposes ERS as a molecular bridge for integrating traditional Chinese and Western medicine in DMC treatment. Future research should leverage emerging technologies such as network pharmacology，multi-omics analysis，and nano-formulations to establish a synergistic network combining modern hypoglycemic drugs and TCM regulation of ERS. This approach is expected to achieve dual efficacy，enhance drug targeting and bioavailability，deepen the understanding of scientific connotation of TCM，and pave new avenues for the prevention and treatment of DMC.关键词：diabetic microvascular complications;endoplasmic reticulum stress （ERS）;apoptosis;autophagy;traditional Chinese medicine24|11|0更新时间：2026-09-16
- 摘要：This study systematically dissects the core pathogenesis of chronic heart failure （CHF） featured by internal deficiency and external excess，imbalance of Qi，blood，Yin，and Yang，and intermingling of phlegm，blood stasis，and fluid retention. According to the traditional Chinese medicine （TCM） therapeutic principles of simultaneously treating root cause and symptoms，regulating Yin and Yang，replenishing Qi and activating blood，and promoting urination to relieve edema，this article deeply explores the formula-syndrome correspondence of Qili Qiangxin （QLQX） capsules in the treatment of CHF，providing a solid theoretical basis for the multi-effect characteristics of this drug. CHF is a common critical cardiovascular disease in clinical practice，and its pathological process involves multiple links including myocardial injury，neurohumoral disturbance，and ventricular remodeling. Its TCM pathogenesis is complex and involves multiple Zang-Fu organs，making it difficult for a single therapeutic method to achieve comprehensive coverage. QLQX capsules，formulated based on classical TCM theory，perfectly matches the pathogenic characteristics of CHF. Modern pharmacological studies have confirmed that QLQX capsules possess definite cardiotonic，diuretic，and vasodilatory effects. The active ingredients of QLQX capsules can rapidly and effectively alleviate the core clinical symptoms such as chest tightness，shortness of breath，decreased exercise tolerance，limb edema，palpitations，and fatigue of CHF patients by enhancing myocardial contractility and coronary blood flow，improving renal water excretion function，dilating peripheral blood vessels，and reducing cardiac load，thereby significantly improving patients' quality of life. On the basis of analyzing the symptomatic treatment of CHF with QLQX capsules，this study further expounds that the drug can intervene in ventricular remodeling through multiple pathways and targets，regulate the pathological mechanism of CHF，improve vascular endothelial function，mediate the activation of related signaling pathways，inhibit the transdifferentiation of cardiac fibroblasts，and regulate myocardial energy metabolism，thus delaying disease progression. QLQX capsules exert significant benefits in reducing composite cardiac events，improving New York Heart Association （NYHA） cardiac function classification，left ventricular ejection fraction （LVEF），6-minute walking distance （6MWD），and quality of life，demonstrating favorable clinical value. With the TCM pathogenesis of CHF as the guiding principle and modern pharmacology as the evidence，this study systematically clarifies the core advantage of QLQX capsules in treatment based on syndrome differentiation and multi-target synergy through the in-depth integration of TCM theory and modern pharmacology. It provides academic support with both theoretical depth and practical value for TCM intervention in CHF，and contributes TCM wisdom and schemes to the construction of a chronic disease management system with Chinese characteristics.关键词：Qili Qiangxin capsules;chronic heart failure;cardioprotective effect;traditional Chinese medicine51|16|0更新时间：2026-09-16
- 摘要：The active components in traditional Chinese medicine （TCM） generally have problems such as poor solubility and low bioavailability， which seriously restrict their clinical efficacy. In recent years， TCM nano-self-assembly based on the non-covalent interactions between molecules has become the research frontier in this field because it can spontaneously form an orderly structure and improve the insoluble components in the body. Moreover， TCM nano-self-assembly has shown unique advantages in the treatment of fibrosis， inflammatory and immune diseases， infectious diseases， and cancer. This article summarizes the research context， structural system， and potential as a pharmacological substance basis of TCM nano-self-assembly by reviewing recent published studies， with focuses on the application of TCM nano-self-assembly in the treatment of diseases from single components to complex systems. In addition， this article summarizes its advantages， mechanism characteristics， and main challenges faced. At present， this field still faces issues such as insufficient mechanism research， a lack of in-depth understanding of the competitive assembly rules of multiple components， difficulty in quality control， unclear in vivo processes and safety， and obstacles to clinical translation. To address these issues， this article proposes a series of solutions， including introducing molecular dynamics simulation and artificial intelligence to predict assembly behavior， using experimental techniques to analyze non-covalent interactions， establishing a comprehensive evaluation system with multiple indicators， using isotope labeling and in vivo imaging techniques to dynamically track in vivo processes， conducting standardized safety evaluation， promoting the filing of hospital preparations and new drug applications， and strengthening early communication between research and regulation. Finally， this article points out the future development directions， aiming to provide reference for subsequent research and clinical translation.关键词：traditional Chinese medicine;non-covalent interaction;nano-self-assembly;research progress88|37|0更新时间：2026-09-16
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