中国临床医学2026，Vol.33Issue(4)：592-598,7.DOI:10.12025/j.issn.1008-6358.2026.20260426
芪苈强心通过调控miR-21-5p/PTEN/PI3K/Akt通路减轻心肌细胞凋亡
Qiliqiangxin attenuates apoptosis of cardiomyocytes by modulating miR-21-5p/PTEN/PI3K/Akt pathway
摘要
Abstract
Objective To explore the mechanism of Qiliqiangxin protecting the cardiomyocytes against oxidative stress.Methods H9C2 cells were exposed to hydrogen peroxide(H2O2)to establish an oxidative stress-induced injury model and were divided into four groups:control group,H2O2 injury group,Qiliqiangxin rescue group(post-injury),and Qiliqiangxin prevention group(pre-treatment).Cell viability was assessed using cell counting Kit-8(CCK-8)assay.Apoptosis rates were measured by flow cytometry.The expression of miR-21-5p was quantified using RT-qPCR.The levels of B-cell lymphoma-2(Bcl-2),Bcl-2-associated X protein(Bax),phosphatase and tensin homolog(PTEN),phosphoinositide 3-kinase(PI3K),protein kinase B(Akt),and phosphorylated Akt(p-Akt)were evaluated by Western blot analysis.Results H2O2 significantly reduced cell viability and increased apoptosis of H9C2 cells(P＜0.05).No statistically significant difference was observed in the Qiliqiangxin rescue group.However,Qiliqiangxin pre-treatment markedly enhanced cell viability and reduced apoptotic rates compared with the H2O2 injury group(P＜0.05).These protective effects were associated with downregulation of PTEN and upregulation of Bcl-2/Bax ratio,miR-21-5p,PI3K,and p-Akt/Akt ratio.Conclusions Qiliqiangxin can protect H9C2 cells against oxidative stress-induced injury,which may be associated with regulation of miR-21-5p/PTEN/PI3K/Akt signaling pathway.关键词
芪苈强心/氧化应激/心肌细胞/miR-21-5p/PTEN/PI3K/Akt信号通路Key words
Qiliqiangxin/oxidative stress/cardiomyocyte/miR-21-5p/PTEN/PI3K/Akt signaling pathway分类
医药卫生引用本文复制引用
连晓雨,龚辉,王旭阳..芪苈强心通过调控miR-21-5p/PTEN/PI3K/Akt通路减轻心肌细胞凋亡[J].中国临床医学,2026,33(4):592-598,7.基金项目
上海市金山区卫生健康委员会科研课题计划青年项目(JSKJ-KTQN-2024-01).Supported by Youth Project of the Research Project Plan of the Health Commission of Jinshan District,Shanghai(JSKJ-KTQN-2024-01). （JSKJ-KTQN-2024-01）
