Article(id=1276976021320630325, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276975955985961244, articleNumber=null, orderNo=null, doi=10.19540/j.cnki.cjcmm.20250728.301, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1748275200000, receivedDateStr=2025-05-27, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1782384408550, onlineDateStr=2026-06-25, pubDate=1767196800000, pubDateStr=2026-01-01, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1782384408550, onlineIssueDateStr=2026-06-25, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1782384408550, creator=13701087609, updateTime=1782384408550, updator=13701087609, issue=Issue{id=1276975955985961244, tenantId=1146029695717560320, journalId=1276577828834349082, year='2026', volume='51', issue='1', pageStart='1', pageEnd='300', issueExtLink='null', onlineDate='null', pubDate='1767196800000', pubDateStr='2026-01-01', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1782384392973, creator='13701087609', updateTime=1782384484405, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1276976339546673871, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276975955985961244, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1276976339546673872, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276975955985961244, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=221, endPage=231, ext={EN=ArticleExt(id=1276976021496791095, articleId=1276976021320630325, tenantId=1146029695717560320, journalId=1276577828834349082, language=EN, title=Protective effect of Renshen-Danshen on myocardial ischemia-reperfusion injury in rats based on SIRT3/PGC-1α/VDAC1 signaling pathway, columnId=null, journalTitle=Chinese Journal of Traditional Chinese Medicine, columnName=null, runingTitle=null, highlight=null, articleAbstract=

This study investigates the mechanisms and target sites of Renshen (Ginseng Radix et Rhizoma)-Danshen (Salviae Miltiorrhizae Radix et Rhizoma) (RSDS) in regulating myocardial ischemia-reperfusion injury (MIRI) via the silent information regulator 3 (SIRT3)/peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α)/voltage-dependent anion-selective channel 1 (VDAC1) signaling pathway. A rat MIRI model was established and randomly divided into control, model, fosinopril, and low-, medium-, and high-dose RSDS groups. Cardiac function, cell apoptosis, and myocardial fibrosis were assessed using cardiac ultrasound, TUNEL staining, hematoxylin-eosin (HE) staining, and Masson staining. Serum factors and the expression of key proteins and genes, such as SIRT3, PGC-1α, and VDAC1 in myocardial tissue, were analyzed using ELISA, Western blot, and RT-qPCR to investigate the underlying mechanisms through the SIRT3/PGC-1α/VDAC1 signaling pathway. The experimental results showed that, compared with the model group, RSDS significantly improved cardiac function, with the high-dose group exhibiting the most pronounced cardioprotective effect, including increased left ventricular ejection fraction (LVEF), decreased left ventricular end-systolic diameter (LVESD), and increased left ventricular fractional shortening (LVFS). TUNEL staining demonstrated that RSDS reduced myocardial cell apoptosis, and Masson staining indicated that RSDS significantly alleviated myocardial fibrosis. Serum levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), C-reactive protein (CRP), and creatine kinase-MB (CK-MB) were significantly decreased, while superoxide dismutase (SOD) levels were significantly increased, suggesting strong anti-inflammatory and antioxidant effects. Western blot and RT-qPCR analyses demonstrated that RSDS improved mitochondrial function, inhibited oxidative stress, and protected myocardial cells by regulating the SIRT3/PGC-1α/VDAC1 signaling pathway. In conclusion, RSDS significantly ameliorates cardiac dysfunction induced by MIRI through regulation of the SIRT3/PGC-1α/VDAC1 signaling pathway, reducing myocardial apoptosis, fibrosis, and inflammation.

, authors=null, authorsList=Qing-zhi RAN, Heng-wen CHEN, authorCompany=null, correspAuthors=Heng-wen CHEN, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1276976021727477817, articleId=1276976021320630325, tenantId=1146029695717560320, journalId=1276577828834349082, language=CN, title=基于SIRT3/PGC-1α/VDAC1信号通路探讨人参-丹参药对对心肌缺血再灌注损伤大鼠的保护作用, columnId=1276975994707775974, journalTitle=中国中药杂志, columnName=药理, runingTitle=null, highlight=null, articleAbstract=

基于沉默信息调节因子2相关酶类3（SIRT3）/过氧化物酶体增殖物激活受体γ-辅激活因子-1α（PGC-1α）/电压依赖性阴离子通道1（VDAC1）信号通路探讨人参-丹参（RSDS）调节心肌缺血再灌注损伤（MIRI）的机制及作用靶点。该研究通过构建大鼠MIRI模型，随机分为对照组，模型组，福辛普利组，人参-丹参低、中、高剂量组。通过心脏超声检查、细胞凋亡（TUNEL）染色、苏木素-伊红（HE）与马松（Masson）染色等方法评估心脏功能、细胞凋亡、心肌纤维化等指标。此外，采用ELISA、Western blot及RT-qPCR技术分析血清因子及心肌组织中SIRT3、PGC-1α、VDAC1等关键蛋白和基因的变化，并基于SIRT3/PGC-1α/VDAC1信号通路研究其作用机制。实验结果表明，与模型组相比，人参-丹参显著改善了心脏功能，尤其是人参-丹参高剂量表现出最强的心脏保护作用，显著升高左心室射血分数（LVEF），显著减小左心室舒张末期内径（LVESD），显著提高左心室短轴缩短率（LVFS）。TUNEL染色显示，人参-丹参能够减少心肌细胞的凋亡。Masson染色结果表明，人参-丹参能够显著减轻心肌纤维化。血清中的白细胞介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）、C反应蛋白（CRP）、肌酸激酶同工酶MB（CK-MB）因子显著下降，而超氧化物歧化酶（SOD）水平显著提高，提示人参-丹参具有较强的抗炎和抗氧化作用。Western blot和RT-qPCR结果表明，人参-丹参通过调节SIRT3/PGC-1α/VDAC1信号通路，显著改善线粒体功能，抑制氧化应激，保护心肌细胞。该研究表明，人参-丹参通过调节SIRT3/PGC-1α/VDAC1信号通路，在多方面显著改善MIRI引起的心脏功能衰竭，减轻心肌细胞凋亡、心肌纤维化及炎症反应。

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冉清智，硕士研究生，E-mail: rqz20010203@126.com

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