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紫草素调控PTEN/AKT/TFEB信号通路改善心肌梗死大鼠心室重构

徐乐 刘纬 陈伟广 温德惠

中国医科大学学报2026,Vol.55Issue(8):728-733,6.
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中国医科大学学报2026,Vol.55Issue(8):728-733,6.DOI:10.12007/j.issn.0258-4646.2026.08.009

紫草素调控PTEN/AKT/TFEB信号通路改善心肌梗死大鼠心室重构

Shikonin modulates PTEN/AKT/TFEB signaling pathway to improve ventricular remodeling in myocardial infarction rats

徐乐 1刘纬 2陈伟广 2温德惠1

作者信息

  • 1. 河北北方学院附属第一医院 超声医学科,河北 张家口 075000
  • 2. 河北北方学院附属第一医院 心血管内科,河北 张家口 075000
  • 折叠

摘要

Abstract

Objective To investigate the mechanism by which shikonin(SK)improves ventricular remodeling in myocardial infarc-tion(MI)by modulating the phosphatase and tensin homolog(PTEN)/protein kinase B(AKT)/transcription factor EB(TFEB)signaling pathway.Methods SD rats were randomly divided into Sham,MI,L-SK,H-SK,and H-SK+BpV groups(n=10 each).Cardiac function,myocardial histopathology,serum inflammatory factor levels,and protein expressions were assessed via echocardiography,histological staining,ELISA,and Western blotting.Results Compared with Sham group,MI group exhibited increased myocardial fibrosis,inflamma-tory infiltration,and deteriorated cardiac function.Compared with the MI group,SK-treated groups(L-SK,H-SK)showed reduced myocar-dial injury and fibrosis,and improved cardiac function in a dose-dependent manner,along with significant changes in PTEN/AKT/TFEB and autophagy-related proteins.The H-SK+BpV group demonstrated opposite trends.Conclusion SK may improve cardiac function and attenuate myocardial injury and fibrosis in MI rats by modulating the PTEN/AKT/TFEB signaling pathway,suppressing inflammation,and activating cardiomyocyte autophagy.

关键词

紫草素/心肌梗死/心室重构/PTEN/AKT/TFEB信号通路/自噬/炎症

Key words

shikonin/myocardial infarction/ventricular remodeling/PTEN/AKT/TFEB signaling pathway/autophagy/inflammation

分类

医药卫生

引用本文复制引用

徐乐,刘纬,陈伟广,温德惠..紫草素调控PTEN/AKT/TFEB信号通路改善心肌梗死大鼠心室重构[J].中国医科大学学报,2026,55(8):728-733,6.

基金项目

河北省医学科学研究课题计划(20211139) (20211139)

中国医科大学学报

0258-4646

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