Article(id=1304388141704569119, tenantId=1146029695717560320, journalId=1302319053441957962, issueId=1304388108988997783, articleNumber=null, orderNo=null, doi=10.7501/j.issn.0253-2670.2026.12.015, pmid=null, cstr=null, oa=null, hot=0, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1770912000000, receivedDateStr=2026-02-13, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1788919967341, onlineDateStr=2026-09-09, pubDate=null, pubDateStr=null, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1788919967341, onlineIssueDateStr=2026-09-09, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1788919967341, creator=13701087609, updateTime=1788919967341, updator=13701087609, issue=Issue{id=1304388108988997783, tenantId=1146029695717560320, journalId=1302319053441957962, year='2026', volume='57', issue='12', pageStart='4509', pageEnd='4948', issueExtLink='null', onlineDate='null', pubDate='1782576000000', pubDateStr='2026-06-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1788919959542, creator='13701087609', updateTime=1788923461082, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1304402795579330582, tenantId=1146029695717560320, journalId=1302319053441957962, issueId=1304388108988997783, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1304402795579330583, tenantId=1146029695717560320, journalId=1302319053441957962, issueId=1304388108988997783, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=4693, endPage=4707, ext={EN=ArticleExt(id=1304388143189352738, articleId=1304388141704569119, tenantId=1146029695717560320, journalId=1302319053441957962, language=EN, title=Linggui Zhugan Decoction improves heart failure after myocardial infarction in rats by restoring mitophagy homeostasis via regulating MCU-mtCa2+ pathway, columnId=null, journalTitle=Chinese Traditional and Herbal Drugs, columnName=null, runingTitle=null, highlight=null, articleAbstract=Objective To investigate the molecular mechanism by which Linggui Zhugan Decoction (苓桂术甘汤, LGZGD) ameliorates heart failure (HF) after myocardial infarction (MI) via regulating mitophagy mediated by mitochondrial calcium uniporter (MCU)-mitochondrial calcium (mtCa2+ ) signaling pathway. Methods Rat models of post-MI HF and hydrogen peroxide (H2 O2 )-induced H9c2 cardiomyocyte injury models were established. For in vivo experiments, rats were assigned to sham group, model group, LGZGD group and captopril group. For in vitro experiments, H9c2 cells were divided into corresponding groups with additional interventions of MCU knockdown or overexpression. Echocardiography, Masson staining and transmission electron microscopy were performed to evaluate rat cardiac function, myocardial fibrosis and mitochondrial ultrastructure, respectively. The mRNA and protein expression levels of genes related to mitophagy and mitochondrial function were detected by qRT-PCR and Western blotting. The levels of reactive oxygen species (ROS) and mtCa2+ were measured, myocardial injury markers were quantitatively analyzed, and changes in cellular autophagic flux were observed using confocal laser scanning microscopy. Results Compared with sham group, rats with post-MI HF exhibited significantly impaired cardiac function, aggravated myocardial fibrosis and mitochondrial damage, dysregulated transcription of mitophagy-related genes, and markedly upregulated MCU transcription level (P < 0.001). In H2 O2 -stimulated H9c2 cells, ROS and mtCa2+ levels were significantly increased, autophagic flux was blocked, and myocardial injury marker levels were notably elevated (P < 0.01).Compared with model group, LGZGD treatment significantly improved cardiac function, alleviated myocardial fibrosis and mitochondrial damage, downregulated MCU expression (P < 0.01), regulated the mRNA expressions of autophagy and mitophagy-related genes in post-MI HF rats (P < 0.05, 0.01). At the cellular level, LGZGD reduced ROS and mtCa2+ levels in H2 O2 -injured H9c2 cells, restored mitochondrial morphology and autophagic flux, and decreased myocardial injury marker levels (P < 0.01). MCU knockdown enhanced the cardioprotective effect of LGZGD, whereas MCU overexpression exacerbated cellular injury. LGZGD effectively reversed MCU overexpression-induced cellular damage and ameliorated the dysregulation of oxidative stress-related enzymes (P < 0.05, 0.01). Conclusions LGZGD alleviates oxidative stress injury and improves post-MI heart failure by restoring MCU-mtCa2+ homeostasis and promoting mitochondrial autophagic flux., authors=WANG Rong, WANG Fang, HUANG Shengyi, HUANG Jinling, authorsList=WANG Rong, WANG Fang, HUANG Shengyi, HUANG Jinling, authorCompany=null, correspAuthors=null, 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=1304388143088689441, articleId=1304388141704569119, tenantId=1146029695717560320, journalId=1302319053441957962, language=CN, title=苓桂术甘汤通过调节MCU-mtCa²⁺通路恢复线粒体自噬稳态改善大鼠心肌梗死后心力衰竭, columnId=1304140191707456168, journalTitle=中草药, columnName=药理与临床, runingTitle=null, highlight=null, articleAbstract=目的 探讨苓桂术甘汤（Linggui Zhugan Decoction，LGZGD）通过调控线粒体钙单向转运体（mitochondrial calcium uniporter，MCU）-线粒体钙（mitochondrial calcium，mtCa²⁺）通路介导的线粒体自噬，改善心肌梗死（myocardial infarction，MI）后心力衰竭（heart failure，HF）的分子机制。方法 构建大鼠MI后HF模型及H₂O₂诱导的H9c2心肌细胞损伤模型，设置假手术组、模型组、LGZGD组和卡托普利组，并结合MCU敲低或过表达进行干预；采用超声心动图、Masson染色、透射电子显微镜分别检测大鼠心功能、心肌纤维化程度、线粒体超微结构，通过qRT-PCR、Western blotting检测线粒体自噬及线粒体功能相关基因和蛋白的表达水平，检测活性氧（reactive oxygen species，ROS）、mtCa²⁺水平并定量分析心肌损伤标志物，利用共聚焦显微镜观察细胞自噬流变化。结果 与假手术组比较，MI后HF大鼠心功能显著下降，心肌纤维化和线粒体损伤加重，线粒体自噬相关基因转录失调，MCU 转录水平显著上调（P ＜0.001）；H₂O₂诱导的H9c2细胞ROS、mtCa²⁺水平显著升高，自噬流受阻，心肌损伤标志物水平显著上升（P ＜0.01）。与模型组比较，LGZGD组可显著改善MI后HF大鼠心功能，减轻心肌纤维化和线粒体损伤，下调MCU 表达（P ＜0.01），调控自噬及线粒体自噬相关基因表达（P ＜0.05、0.01）；细胞水平上LGZGD可降低H₂O₂诱导的H9c2细胞ROS、mtCa²⁺水平，恢复线粒体形态和自噬流，降低心肌损伤标志物水平（P ＜0.01）。MCU敲低可增强LGZGD的心脏保护效果，MCU过表达则加剧细胞损伤，LGZGD可有效逆转MCU过表达造成的细胞损伤，并改善氧化应激相关酶紊乱（P ＜0.05、0.01）。结论 LGZGD通过恢复MCU-mtCa²⁺稳态、促进线粒体自噬流，减轻氧化应激损伤，改善MI后HF。, authors=王荣1 , 王芳1,2 , 黄圣意1 , 黄金玲1 , authorsList=王荣, 王芳, 黄圣意, 黄金玲, authorCompany=1 安徽中医药大学中西医结合学院,安徽 合肥 230012; 2+ overload in chronic postischemic cardiac remodeling [J]. Cell Death Differ, 2020, 27(6): 1907-1923.2 O2 诱导的H9c2细胞损伤[J]. 中国实验方剂学杂志, 2022, 28(13): 1-9.
中草药
|药理与临床
2026
, 57
(12) :
4693
-4707
苓桂术甘汤通过调节MCU-mtCa²⁺通路恢复线粒体自噬稳态改善大鼠心肌梗死后心力衰竭
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作者信息
通讯作者:
黄金玲
作者简介:
王荣: 王荣，博士研究生，从事中药复方效用机制与物质基础研究。E-mail:wr976016756@163.com
Linggui Zhugan Decoction improves heart failure after myocardial infarction in rats by restoring mitophagy homeostasis via regulating MCU-mtCa2+ pathway
Affiliations
doi: 10.7501/j.issn.0253-2670.2026.12.015
文章导航
目的 探讨苓桂术甘汤（Linggui Zhugan Decoction，LGZGD）通过调控线粒体钙单向转运体（mitochondrial calcium uniporter，MCU）-线粒体钙（mitochondrial calcium，mtCa²⁺）通路介导的线粒体自噬，改善心肌梗死（myocardial infarction，MI）后心力衰竭（heart failure，HF）的分子机制。方法 构建大鼠MI后HF模型及H₂O₂诱导的H9c2心肌细胞损伤模型，设置假手术组、模型组、LGZGD组和卡托普利组，并结合MCU敲低或过表达进行干预；采用超声心动图、Masson染色、透射电子显微镜分别检测大鼠心功能、心肌纤维化程度、线粒体超微结构，通过qRT-PCR、Western blotting检测线粒体自噬及线粒体功能相关基因和蛋白的表达水平，检测活性氧（reactive oxygen species，ROS）、mtCa²⁺水平并定量分析心肌损伤标志物，利用共聚焦显微镜观察细胞自噬流变化。结果 与假手术组比较，MI后HF大鼠心功能显著下降，心肌纤维化和线粒体损伤加重，线粒体自噬相关基因转录失调，MCU 转录水平显著上调（P ＜0.001）；H₂O₂诱导的H9c2细胞ROS、mtCa²⁺水平显著升高，自噬流受阻，心肌损伤标志物水平显著上升（P ＜0.01）。与模型组比较，LGZGD组可显著改善MI后HF大鼠心功能，减轻心肌纤维化和线粒体损伤，下调MCU 表达（P ＜0.01），调控自噬及线粒体自噬相关基因表达（P ＜0.05、0.01）；细胞水平上LGZGD可降低H₂O₂诱导的H9c2细胞ROS、mtCa²⁺水平，恢复线粒体形态和自噬流，降低心肌损伤标志物水平（P ＜0.01）。MCU敲低可增强LGZGD的心脏保护效果，MCU过表达则加剧细胞损伤，LGZGD可有效逆转MCU过表达造成的细胞损伤，并改善氧化应激相关酶紊乱（P ＜0.05、0.01）。结论 LGZGD通过恢复MCU-mtCa²⁺稳态、促进线粒体自噬流，减轻氧化应激损伤，改善MI后HF。
苓桂术甘汤
/
心力衰竭
/
线粒体自噬
/
线粒体钙单向转运体
/
氧化应激
/
茯苓酸B
/
肉桂酸
/
白术内酯III
/
甘草次酸
Objective To investigate the molecular mechanism by which Linggui Zhugan Decoction (苓桂术甘汤, LGZGD) ameliorates heart failure (HF) after myocardial infarction (MI) via regulating mitophagy mediated by mitochondrial calcium uniporter (MCU)-mitochondrial calcium (mtCa2+ ) signaling pathway. Methods Rat models of post-MI HF and hydrogen peroxide (H2 O2 )-induced H9c2 cardiomyocyte injury models were established. For in vivo experiments, rats were assigned to sham group, model group, LGZGD group and captopril group. For in vitro experiments, H9c2 cells were divided into corresponding groups with additional interventions of MCU knockdown or overexpression. Echocardiography, Masson staining and transmission electron microscopy were performed to evaluate rat cardiac function, myocardial fibrosis and mitochondrial ultrastructure, respectively. The mRNA and protein expression levels of genes related to mitophagy and mitochondrial function were detected by qRT-PCR and Western blotting. The levels of reactive oxygen species (ROS) and mtCa2+ were measured, myocardial injury markers were quantitatively analyzed, and changes in cellular autophagic flux were observed using confocal laser scanning microscopy. Results Compared with sham group, rats with post-MI HF exhibited significantly impaired cardiac function, aggravated myocardial fibrosis and mitochondrial damage, dysregulated transcription of mitophagy-related genes, and markedly upregulated MCU transcription level (P < 0.001). In H2 O2 -stimulated H9c2 cells, ROS and mtCa2+ levels were significantly increased, autophagic flux was blocked, and myocardial injury marker levels were notably elevated (P < 0.01).Compared with model group, LGZGD treatment significantly improved cardiac function, alleviated myocardial fibrosis and mitochondrial damage, downregulated MCU expression (P < 0.01), regulated the mRNA expressions of autophagy and mitophagy-related genes in post-MI HF rats (P < 0.05, 0.01). At the cellular level, LGZGD reduced ROS and mtCa2+ levels in H2 O2 -injured H9c2 cells, restored mitochondrial morphology and autophagic flux, and decreased myocardial injury marker levels (P < 0.01). MCU knockdown enhanced the cardioprotective effect of LGZGD, whereas MCU overexpression exacerbated cellular injury. LGZGD effectively reversed MCU overexpression-induced cellular damage and ameliorated the dysregulation of oxidative stress-related enzymes (P < 0.05, 0.01). Conclusions LGZGD alleviates oxidative stress injury and improves post-MI heart failure by restoring MCU-mtCa2+ homeostasis and promoting mitochondrial autophagic flux.
Linggui Zhugan Decoction
/
heart failure
/
mitophagy
/
mitochondrial calcium uniporter
/
oxidative stress
/
pachymic acid B
/
cinnamic acid
/
atractylenolide III
/
glycyrrhetinic acid
王荣, 王芳, 黄圣意, 黄金玲.
苓桂术甘汤通过调节MCU-mtCa²⁺通路恢复线粒体自噬稳态改善大鼠心肌梗死后心力衰竭.
中草药,
2026
, 57
(12)
: 4693
-4707
.
DOI: 10.7501/j.issn.0253-2670.2026.12.015
WANG Rong, WANG Fang, HUANG Shengyi, HUANG Jinling.
Linggui Zhugan Decoction improves heart failure after myocardial infarction in rats by restoring mitophagy homeostasis via regulating MCU-mtCa2+ pathway[J].
Chinese Traditional and Herbal Drugs ,
2026
, 57
(12)
: 4693
-4707
.
DOI: 10.7501/j.issn.0253-2670.2026.12.015
国家自然科学基金资助项目 (81973844); 安徽省重点研究与开发计划项目 (201904a07020109); 安徽中医药大学研究生科技创新基金资助项目 (2021ZC09); 黄金玲安徽省名中医工作室 (2025)
参考文献
引证文献
Udell J A, Bahit M C, Campbell P, et al. Prevention of heart failure after acute myocardial infarction [J]. Lancet, 2025, 406(10508): 1154-1170.2+ overload in chronic postischemic cardiac remodeling [J]. Cell Death Differ, 2020, 27(6): 1907-1923.2 O2 诱导的H9c2细胞损伤[J]. 中国实验方剂学杂志, 2022, 28(13): 1-9.
2026年第57卷第12期
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doi: 10.7501/j.issn.0253-2670.2026.12.015
接收时间：2026-02-13
首发时间：2026-09-09
https://castjournals.cast.org.cn/joweb/zcy/CN/10.7501/j.issn.0253-2670.2026.12.015
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2种不同金属材料的力学参数
科 属数 种数 占总种数比例 属 种数 占总种数比例 鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78 小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39 多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39 红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87 小菇属 Mycena 11 5.26 光柄菇属 Pluteus 5 2.39 红菇属 Russula 17 8.13 栓菌属 Trametes 5 2.39
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