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Editor-in-Chief：WU Yiling
Supervisor：

National Administration of Traditional Chinese Medicine
Sponsor：

Institute of Traditional Chinese Medicine，China Academy of Chinese Medical Sciences；China Association of Chinese Medicine

CN：11-3495/R

ISSN：1005-9903（Print）

ISSN：2097-1494（Online）

IF：5.474（CNKI）

Publication Cycle：Semimonthly

Address：No.16，Nanxiao Street，Dongzhimen，Dongcheng District，Beijing

Tel：010-84076882

E-mail：syfjx_2010@188.com

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Danlianxin Formula Ameliorates Cardiac Dysfunction Associated with Myocardial Infarction in Hyperlipidemic Rats via Epac1/VDAC1/NLRP3/Caspase Signaling Pathway

ObjectiveTo investigate the improvement effect and mechanism of Danlianxin formula （DLXF） on cardiac function associated with myocardial infarction （MI） in hyperlipidemic rats.MethodsThe hyperlipidemia model was established by feeding rats a high-fat diet for 8 weeks， followed by the MI modeling induced by ligating the left anterior descending coronary artery. After 4 weeks of gavage administration of DLXF at low （1.108 g·kg-1·d-1） and high （2.217 g·kg-1·d-1） doses， the following assessments were conducted： Observation of physical signs， echocardiography for cardiac function， histopathological examination for cardiac morphology， laser speckle contrast imaging for mesenteric microvascular perfusion， serum biochemical tests for key lipid parameters such as total cholesterol （TC） and triglycerides （TG）， as well as inflammatory cytokines including interleukin-1β （IL-1β）， IL-6， N-terminal pro-brain natriuretic peptide （NT-proBNP）， and tumor necrosis factor-α （TNF-α）， and Real-time PCR and Western blot analysis for the expression of cAMP-regulated guanine nucleotide exchange factor 1 （Epac1）， voltage-dependent anion channel 1 （VDAC1）， NOD-like receptor thermal protein domain associated protein 3 （NLRP3）， cysteinyl aspartate-specific proteinase （Caspase）-9， and Caspase-3.ResultsThe survival status of rats was generally improved in the DLXF group. Echocardiography revealed that compared with the model group， the high-dose DLXF group exhibited increased left ventricular ejection fraction （LVEF） and left ventricular short-axis shortening fraction （LVFS）， while both DLXF groups showed reduced left ventricular internal diameter at end-diastole （LVIDd） and left ventricular internal diameter at end-systole （LVIDs） （P<0.01）. Dynamic laser speckle flow imaging revealed reduced blood flow in the hyperlipidemia model group compared with the normal group （P<0.05）. Compared with that in the model group， mesenteric blood flow was increased in all drug treatment groups （P<0.01）. Serum biochemical test results showed that compared with those in the model group， both TC and TG levels were decreased in the low-dose DLXF group （P<0.05）， and the TG level was decreased in the high-dose group （P<0.05）. Both DLXF groups showed elevated high-density lipoprotein cholesterol （HDL-C） levels （P<0.05， P<0.01） and declined very low-density lipoprotein （VLDL） levels （P<0.01）， and the high-dose DLXF group exhibited a decreased low-density lipoprotein cholesterol （LDL-C） level （P<0.01）. enzyme-linked immunosorbent assay （ELISA） results showed that compared with those in the normal group， the IL-1β， IL-6， TNF-α， and NT-proBNP levels were elevated in the hyperlipidemia model group （P<0.01）. Compared with the model group， both DLXF groups showed a declining trend in serum IL-1β， IL-6， and TNF-α levels （P<0.05， P<0.01） and reduced NT-proBNP levels （P<0.01）. Histopathological findings revealed improved myocardial structure， regular fiber arrangement， reduced inflammatory infiltration， and diminished collagen proliferation in DLXF groups compared with the model group. Ultrastructural analysis of mitochondria demonstrated well-organized myocardial cell structure， orderly myofibrillar arrangement， and improved mitochondrial alignment with clear structure in DLXF groups compared with the model group. Myocardial cell apoptosis analysis revealed disordered cell arrangement and scattered brown apoptotic cells in the hyperlipidemia model group， with a higher number of apoptotic cells than the sham operation group. Compared with the model group， DLXF groups exhibited scattered apoptosis of varying degrees， altered cell morphology， and reduced apoptosis. Real-time PCR and Western blot results indicated that compared with the model group， DLXF downregulated the protein and mRNA levels of Epac1， VDAC1， NLRP3， Caspase-9， and Caspase-3 （P<0.05， P<0.01）.ConclusionDLXF can modulate the Epac1/VDAC1/NLRP3/Caspase signaling pathway to improve the mitochondrial structure and function and suppress inflammation， thereby enhancing cardiac function in myocardial infarction （MI） in hyperlipidemic rats.

XIANG Chunrong, MA Jingzhuo, HE Xuanhui, CHEN Hengwen

Danlianxin Formula Ameliorates Cardiac Dysfunction Associated with Myocardial Infarction in Hyperlipidemic Rats via Epac1/VDAC1/NLRP3/Caspase Signaling Pathway
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Volume 32 期 13，2026 2026年第32卷第13期

    LIU Yuxi, ZHU Zhongkang, WANG Songnan, LIU Jiali, YIN Ye, MIAO Jiarui, HE Shunuo, ZHAO Danyu

    Vol. 32, Issue 13, Pages: 1-10(2026) DOI: 10.13422/j.cnki.syfjx.20252402
    摘要：ObjectiveThis study aims to investigate the effect of Liuwei Dihuangwan on the autophagy function in the hippocampus of senescence-accelerated mouse prone 8 （SAMP8） by regulating the expression of glycoprotein non-metastatic melanoma protein B （GPNMB）. Furthermore， it is designed to explore the mechanism of the method of tonifying the kidneys and replenishing essence in the treatment of Alzheimer's disease （AD）.MethodsIn experiment 1， 24 5-month-old SAMP8 mice were randomly and equally divided into the model group， and the low-， middle- and high-dose（0.59，1.18，2.36 g·kg-1） Liuwei Dihuangwan groups. At the same time， six 5-month-old senescence accelerated mouse resistant 1 （SAMR1） mice were used as the control group. The learning and memory ability was evaluated through novel object recognition experiment. Serum cortisol （Cort）， adrenocorticotropic hormone （ACTH） and urine 17-hydroxycorticosteroid （17-OHCS） levels were detected by enzyme-linked immunosorbent assay （ELISA）. The ultrastructure of hippocampal neurons was observed by transmission electron microscope （TEM）， and the expression levels of hippocampal GPNMB， a disintegrin and metalloproteinase 10 （ADAM10） and autophagy-related proteins were detected by Western blot. In experiment 2， 18 SAMP8 mice were randomly and equally divided into the model group， vector control group （Vector）， and GPNMB overexpression group （GPNMBOE）. Lentiviral vectors were stereotactically injected into the brain （2 μL per side in the GPNMBOE group）. Western blot was used to detect the expression of the above target proteins in the hippocampus； In Experiment 3， 24 SAMP8 mice were randomly and equally divided into the model group， Liuwei Dihuangwan group， Liuwei Dihuangwan+negative control （NC） group， and Liuwei Dihuangwan+GPNMB silencing group （shGPNMB）. Before drug treatment， the Liuwei Dihuangwan+NC group and the Liuwei Dihuangwan+shGPNMB group were injected with negative control and GPNMB silencing lentivirus， respectively. Western blot was used to detect the expression of the above target proteins in the hippocampus.ResultsThe novel object discrimination index of mice in the model group was significantly lower than that of mice in the control group （P<0.01）. The novel object discrimination index of mice in the medium- and high-dose Liuwei Dihuangwan groups was significantly higher than that of mice in the model group （P<0.01）. Aggregated autolysosomes were observed in the normal hippocampus tissue by TEM. In the model group， mitochondria were dominant， and no typical characteristic autophagosomes were observed. In the low- and medium-dose Liuwei Dihuangwan groups， a small number of autolysosomes and autophagosomes with double-membrane structures were observed. In the high-dose Liuwei Dihuangwan group， the number of autophagosomes and autolysosomes was greater than that in the low- and medium-dose groups. The results of ELISA and Western blot showed that compared with the control group， the levels of serum Cort， ACTH， and urine 17-OHCS in the model group were substantially increased， while the expression of hippocampal ADAM10， Beclin1， and microtubule associated-protein light chain 3-Ⅱ/Ⅰ （LC3 Ⅱ/Ⅰ） was significantly decreased. The expression of GPNMB and ubiquitin binding protein p62 was significantly increased （P<0.05， P<0.01）. Compared with the model group， the serum Cort and ACTH levels in the low-， medium-， and high-dose Liuwei Dihuangwan groups were significantly reduced， while only the urine 17-OHCS level in the high-dose group was significantly reduced. The hippocampal GPNMB， ADAM10， Beclin1， and LC3 Ⅱ/Ⅰ expression levels in the medium-， and high-dose groups of Liuwei Dihuangwan were significantly increased compared to the model group， whereas the expression of p62 was significantly reduced （P<0.01）. The above indicators showed a progressive trend among the three groups. Compared with the model group， the GPNMBOE group showed a significant increase in GPNMB， ADAM10， Beclin1， LC3 Ⅱ/Ⅰ expression， and a significant decrease in p62 expression （P<0.01）. Compared with the model group， the expression of GPNMB， ADAM10， Beclin1， and LC3 Ⅱ/Ⅰ in the hippocampus of the Liuwei Dihuangwan group significantly increased， while the expression of p62 significantly decreased （P<0.01）. Compared with the Liuwei Dihuangwan group， the Liuwei Dihuangwan+shGPNMB group showed a significant decrease in GPNMB， ADAM10， Beclin1， LC3 Ⅱ/Ⅰ， and a significant increase in p62 expression （P<0.01）.ConclusionLiuwei Dihuangwan can enhance hippocampal autophagy function and improve AD by upregulating GPNMB expression.  
    关键词：Alzheimer's disease;Liuwei Dihuangwan;glycoprotein non-metastatic melanoma protein B （GPNMB）;autophagy;tonify the kidneys and replenish essence   
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    CHEN Jiawei, LIU Maohui, YANG Zhida, DING Weijun, XIA Xiuwen

    Vol. 32, Issue 13, Pages: 11-19(2026) DOI: 10.13422/j.cnki.syfjx.20260264
    摘要：ObjectiveThis paper aims to investigate the mechanism by which Erchentang improves body weight in obese mice by regulating the AMP‑activated protein kinase （AMPK）/peroxisome proliferator‑activated receptor γ coactivator‑1α （PGC‑1α） signaling pathway and inducing browning of inguinal white adipose tissue （iWAT）.MethodsObese mouse models were established by feeding a high‑fat diet. After successful modeling， mice were randomly divided into a model group and low‑， medium‑， and high‑dose Erchentang groups （7.5， 15， 30 g·kg-1）， with six mice in each group. Another six normal mice were set as the normal group. Mice in the treatment groups were administered with corresponding doses of the drug by gavage， while those in the normal and model groups were administered with an equal volume of pure water by gavage for four consecutive weeks. Obesity was evaluated by body weight and Lee's index. The levels of low‑density lipoprotein cholesterol （LDL‑C） and high‑density lipoprotein cholesterol （HDL‑C） in serum were detected by biochemical assays. The leptin content in serum was measured by enzyme‑linked immunosorbent assay （ELISA）. Hematoxylin and eosin （HE） staining was used to observe the pathological morphology of the liver and iWAT. Immunofluorescence staining was applied to detect the protein expression levels of glucose transporter 4 （GLUT4） in the liver and iWAT. Molecular docking was performed to simulate the binding affinity between the key components of Erchentang （nobiletin， diosmetin， naringenin） and the key pathway proteins AMPK and PGC‑1α. Western blot was used to detect the protein expression levels of uncoupling protein‑1 （UCP‑1）， AMPK， phosphorylated AMP-activated protein kinase （p‑AMPK）， and PGC‑1α in iWAT.ResultsCompared with those in the normal group， the mice in the model group showed significantly increased body weight and Lee's index， elevated levels of HDL‑C， LDL‑C， and leptin in serum， enlarged adipocytes in iWAT， down‑regulated protein expression levels of GLUT4 in iWAT and liver， and decreased protein expression levels of UCP‑1 and PGC‑1α in iWAT（P<0.05， P<0.01）， the expression level of p-AMPK / AMPK protein was up-regulated， but the difference was not statistically significant. Compared with those in the model group， the mice in the Erchentang groups with different doses exhibited significantly reduced body weight and Lee's index， decreased levels of HDL‑C， LDL‑C， and leptin in serum， smaller adipocytes in iWAT， up‑regulated GLUT4 protein expression levels in iWAT and liver， and increased protein expression levels of UCP‑1， p‑AMPK/AMPK， and PGC‑1α in iWAT （P<0.05， P<0.01）. Molecular docking results show that nobiletin， diosmetin， and naringenin have strong binding energies with both AMPK and PGC‑1α.ConclusionErchentang may improve body weight in obese mice by regulating the AMPK/PGC‑1α signaling pathway and inducing iWAT browning.  
    关键词：obesity;traditional Chinese medicine;Erchentang;browning of white adipose tissue;AMP‑activated protein kinase （AMPK）/peroxisome proliferator‑activated receptor γ coactivator‑1α （AMPK/PGC-1α） signaling pathway   
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    ZHONG Zhen, WEI Dongsheng, XIONG Xinyue, LI Lin, YAO Mingli, SHI Xinnuan, JIANG Youming

    Vol. 32, Issue 13, Pages: 20-31(2026) DOI: 10.13422/j.cnki.syfjx.20260518
    摘要：ObjectiveTo investigate the effects of modified Xiaoyaosan （JJXYS） on behavioral abnormalities and hippocampal mitochondrial quality control （MQC） in the rat model of post-myocardial infarction depression （PMD） and preliminarily explore its potential mechanism.MethodsA rat model of PMD was established by left anterior descending coronary artery ligation combined with chronic unpredictable mild stress （CUMS）. Rats were randomized into a control group， a model group， a fluoxetine （FLX， 10 mg·kg-1） group， and low-， medium-， and high-dose JJXYS （JJXYS-L/M/H， 1.12， 2.24， 4.48 g·kg-1， respectively） groups. Depressive-like behaviors were evaluated by body weight monitoring， sucrose preference test， open field test， and forced swimming test. Hematoxylin-eosin staining and Nissl staining were used to observe hippocampal histomorphology and neuronal changes. Enzyme-linked immunosorbent assay was conducted to determine the serum levels of 5-hydroxytryptamine （5-HT）， dopamine （DA）， interleukin-1 beta （IL-1β）， interleukin-6 （IL-6）， and tumor necrosis factor-alpha （TNF-α）. The mRNA levels of MQC-related genes including peroxisome proliferator-activated receptor-gamma coactivator-1 alpha （PGC-1α）， nuclear respiratory factor 1 （Nrf1）， and transcription factor A， mitochondrial （TFAM） in the hippocampal tissue were measured by real-time PCR. The expression of proteins related to the dynamin-related protein 1 （Drp1）/PTEN-induced putative kinase 1 （PINK1）/Parkin signaling pathway was determined by Western blot.ResultsCompared with the control group， the model group showed restricted body weight gain， aggravated depressive-like behaviors， declined serum 5-HT and DA levels， evident hippocampal neuronal damage and reduced Nissl bodies， as well as downregulated expression of MQC-related genes and proteins （P<0.05）. Compared with the model group， both FLX and JJXYS alleviated the above changes to varying degrees. Moreover， the JJXYS-M and JJXYS-H groups showed more pronounced effects， improving behavioral performance， restoring 5-HT and DA levels， alleviating hippocampal pathological injury， and upregulating the expression of PGC-1α/Nrf1/TFAM mRNA and Drp1/PINK1/Parkin signaling pathway-related proteins （P<0.05）.ConclusionJJXYS can significantly alleviate depressive-like behaviors and neurotransmitter imbalance in the rat model of PMD by regulating hippocampal MQC and upregulating the Drp1/PINK1/Parkin-related pathway. This study provides experimental evidence for the intervention of PMD with JJXYS.  
    关键词：modified Xiaoyaosan;post-myocardial infarction depression;dynamin-related protein 1 （Drp1）/PTEN-induced putative kinase 1 （PINK1）/Parkin;mitochondrial quality control   
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