摘要
研究苍术酮(atractylone,Atr)对H_(2)O_(2)诱导的大鼠心肌细胞H9c2氧化损伤的保护作用及相关机制。首先,利用H_(2)O_(2)诱导H9c2细胞建立心肌细胞氧化损伤模型。通过检测细胞活力、细胞凋亡和氧化应激标志物评估Atr对H9c2细胞氧化损伤的作用。通过生物信息学分析的方法预测Atr发挥作用的分子机制。进一步检测Atr对磷脂酰肌醇3-激酶(phosphatidylinositol 3-kinase,PI3K)/蛋白激酶B(protein kinase B,AKT)信号通路的影响并验证该信号通路是否参与了Atr对H9c2细胞氧化损伤的调控。结果表明,Atr可以显著减轻H9c2细胞的氧化损伤(P<0.05)。PI3K/AKT信号通路可能参与了Atr对H9c2细胞损伤的调控。Atr显著上调了损伤细胞中被抑制的PI3K/AKT信号通路水平(P<0.05),其保护作用可以被通路抑制剂逆转(P<0.05)。综上,Atr可以通过激活PI3K/AKT信号通路对H9c2细胞H_(2)O_(2)氧化损伤发挥保护作用。
The study investigated the protective effects and underlying mechanisms of atractylone(Atr)against H_(2)O_(2)-induced oxidative damage in rat cardiomyocyte H9c2 cells.Initially,an oxidative damage model was established by inducing H9c2 cells with H_(2)O_(2).The effects of Atr against oxidative damage were assessed by measuring cell viability,apoptosis,and oxidative stress markers.Bioinformatics analysis was employed to predict the molecular mechanisms of Atr.Further experiments were conducted to examine the impact of Atr on the phosphatidylinositol 3-kinase(PI3K)/protein kinase B(AKT)signaling pathway and to verify its involvement in the regulation of oxidative damage in H9c2 cells.Results showed that Atr significantly alleviated oxidative damage in H9c2 cells(P<0.05).The PI3K/AKT signaling pathway appears to be involved in the regulation of Atr's protective effects.Atr significantly upregulated the suppressed PI3K/AKT signaling pathway in damaged cells(P<0.05),and its protective effects were reversed by pathway inhibitor(P<0.05).In conclusion,Atr exerts its protective effects against H_(2)O_(2)-induced oxidative damage in H9c2 cells by activating the PI3K/AKT signaling pathway.
作者
张楠楠
王晓玲
郭娟
黄俣佳
黄圣
王丹君
王占吉
ZHANG Nan-nan;WANG Xiao-ling;GUO Juan;HUANG Yu-jia;HUANG Sheng;WANG Dan-jun;WANG Zhan-ji(Key Laboratory of Research on Human Genetic Diseases at Universities of Inner Mongolia Autonomous Region,School of Basic Medicine,Chifeng University,Chifeng 024000,China)
出处
《天然产物研究与开发》
北大核心
2025年第8期1535-1543,共9页
Natural Product Research and Development
基金
赤峰市自然科学科研课题(SZR24001)
赤峰学院第二批博士下基层服务地方项目(2024FWDF10)
赤峰学院2024年度大学生创新创业训练计划(S202410138020)。
关键词
苍术酮
H9C2心肌细胞
氧化损伤
PI3K/AKT信号通路
atractylone
H9c2 cardiomyocytes
oxidative damage
phosphatidylinositol 3-kinase/protein kinase B signaling pathway
作者简介
通信作者:张楠楠,Tel:86-015849652736,E-mail:nannanzhangkjd@163.com。
