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益气活血方对冠心病气虚血瘀证大鼠PI3K/Akt/mTOR信号通路及自噬的影响

何娜祯 贝雪怡 陈光宇 李亮 瞿昊宇 谢梦洲

湖南中医药大学学报2025,Vol.45Issue(11):2035-2043,9.
湖南中医药大学学报2025,Vol.45Issue(11):2035-2043,9.DOI:10.3969/j.issn.1674-070X.2025.11.003

益气活血方对冠心病气虚血瘀证大鼠PI3K/Akt/mTOR信号通路及自噬的影响

Effects of Yiqi Huoxue Formula on PI3K/Akt/mTOR signaling pathway and autophagy in coronary heart disease rats with qi deficiency induced blood stasis pattern

何娜祯 1贝雪怡 1陈光宇 1李亮 1瞿昊宇 2谢梦洲1

作者信息

  • 1. 湖南中医药大学,湖南 长沙 410208||湖南省药食同源功能性食品工程技术研究中心,湖南 长沙 410208||湖南中医药大学中医心肺病证辨证与药膳食疗重点研究室,湖南 长沙 410208||湖南中医药大学中医诊断学湖南省重点实验室,湖南 长沙 410208
  • 2. 湖南中医药大学,湖南 长沙 410208||湖南省药食同源功能性食品工程技术研究中心,湖南 长沙 410208||湖南中医药大学中医心肺病证辨证与药膳食疗重点研究室,湖南 长沙 410208||湖南中医药大学信息科学与工程学院,湖南 长沙 410208
  • 折叠

摘要

Abstract

Objective To investigate the effects of the Yiqi Huoxue Formula(YQHXF)on autophagy and phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin(PI3K/Akt/mTOR)signaling pathway in coronary heart disease(CHD)rats with qi deficiency induced blood stasis pattern,and to clarify its mechanism of action.Methods Forty-eight male SPF-grade SD rats were randomly divided into sham-operated group,model group,YQHXF group(17.1 g·kg-1),and western medicine group(isosorbide mononitrate 3.6 mg·kg-1),with 12 rats in each group.Except the rats of the sham-operated group,models of CHD rats with qi deficiency induced blood stasis pattern were prepared by ligation of left anterior descending coronary artery combined with swimming exhaustion method in the other groups.For the sham-operated group,only threading without ligation was performed.After 14 days of gavage intervention,samples were collected.The general state and changes of electrocardiogram were observed among different groups of rats.The cardiac function was measured by echocardiography,whole blood viscosity by hemorheography,pathological morphology of myocardial tissue by HE staining,myocardial ultrastructure by transmission electron microscopy,mRNA expression levels of Beclin-1,LC3-II,Akt,and mTOR by RT-PCR,protein expressions of Beclin-1,LC3-II,Akt,and mTOR in myocardial tissue by Western blot.Results Compared with the sham-operated group,the model group exhibited worsened general state:elevated ST segment of electrocardiograms(P<0.01),decreased ejection fraction(EF)and fractional shortening(FS)values(P<0.01),increased left ventricular internal end-diastolic diameter(LVIDd)and left ventricular internal end-systolic diameter(LVIDs)(P<0.01),increased whole blood viscosity(P<0.01),disorganized myocardial tissue arrangement,severe myocardial injury,significantly impaired myocardial ultrastructure,up-regulated mRNA and protein expressions of Akt and mTOR(P<0.01),and down-regulated mRNA and protein expressions of Beclin-1 and LC3-Ⅱ(P<0.01).Compared with the model group,the YQHXF group and western medicine group both showed improved general state:decreased ST segment of electrocardiogram(P<0.01),increased EF and FS values(P<0.01),decreased LVIDd and LVIDs(P<0.05,P<0.01),decreased whole blood viscosity(P<0.01),aligned myocardial fibers,improved myocardial cell structure and morphology,ameliorated myocardial ultrastructure impairment,down-regulated mRNA and protein expressions of Akt and mTOR(P<0.05,P<0.01),and up-regulated mRNA and protein expressions of Beclin-1 and LC3-Ⅱ(P<0.05,P<0.01).Conclusion YQHXF can improve cardiac function and ameliorate myocardial injury in CHD rats with qi deficiency induced blood stasis pattern,effectively treating CHD with qi deficiency induced blood stasis pattern.Its mechanism of action may be related to the regulation of PI3K/Akt/mTOR signaling pathway and the activation of autophagy.

关键词

冠心病/益气活血方/气虚血瘀证/PI3K/Akt/mTOR信号通路/自噬

Key words

coronary heart disease/Yiqi Huoxue Formula/qi deficiency induced blood stasis pattern/PI3K/Akt/mTOR signaling pathway/autophagy

分类

医药卫生

引用本文复制引用

何娜祯,贝雪怡,陈光宇,李亮,瞿昊宇,谢梦洲..益气活血方对冠心病气虚血瘀证大鼠PI3K/Akt/mTOR信号通路及自噬的影响[J].湖南中医药大学学报,2025,45(11):2035-2043,9.

基金项目

国家自然科学基金面上项目(82374323) (82374323)

湖南省重点领域研发计划项目(2022SK2124) (2022SK2124)

湖南省教育厅科研项目(19A380) (19A380)

湖南省中医药科研计划项目(202004). (202004)

湖南中医药大学学报

1674-070X

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