遵义医科大学附属医院心血管内科;
目的 探讨骨髓间充质干细胞(BMSCs)来源的外泌体(BMSCs-exosome)微小RNA(miR)-126对缺氧条件下H9c2心肌细胞凋亡的影响及作用机制。方法 采用缺氧24 h建立H9c2心肌细胞缺氧模型[1];提取BMSCs-exosome并鉴定;转染miR-126抑制剂(Inhibitor)及阴性对照(INC)至BMSCs提取exosome(Inhibitor-exo、INC-exo)并与缺氧诱导的H9c2心肌细胞共培养。实验分组:对照(Control)组、缺氧(Hypoxia)组、BMSCs-exosome(BMSCs-exo)组、INC-exo组、Inhibitor-exo组。采用流式细胞术(FCM)、TUNEL试验检测细胞凋亡;实时荧光定量-聚合酶链反应(RT-qPCR)检测BMSCs-exo、INC-exo、Inhibitor-exo处理H9c2心肌细胞后细胞内miR-126的相对表达量;Targetscan数据库预测miR-126作用的下游靶基因磷酸肌醇3激酶调节亚基(PIK3R)2,Western印迹检测PIK3R2及其信号通路相关蛋白磷脂酰肌醇-3激酶(PI3K)、蛋白激酶B(Akt)及磷酸化蛋白p-Akt蛋白表达。结果 与Control组相比,Hypoxia组细胞凋亡明显增多,而在缺氧基础下,BMSCs-exo组细胞凋亡明显减少(P<0.05)。与BMSCs-exo组相比,Inhibitor-exo组细胞凋亡率明显升高(P<0.05)。Western印迹结果显示,Inhibitor-exo组PIK3R2蛋白表达明显增加,PI3K、p-Akt蛋白表达明显降低(P<0.05)。结论 BMSCs-exosome通过传递miR-126至H9c2心肌细胞后抑制PIK3R2表达、激活PI3K/Akt信号通路,从而发挥抗细胞凋亡作用。
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下载次数 | 被引频次 | 阅读次数 |
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基本信息:
DOI:
中图分类号:R542.2
引用信息:
[1]刘围围,韩韦钰,李娇等.骨髓间充质干细胞源外泌体miR-126对缺氧条件下H9c2心肌细胞凋亡的影响及作用机制[J].中国老年学杂志,2025,45(10):2422-2428.
基金信息:
贵州省科技计划项目(黔科合基础-ZK[2022]一般653); 贵州省卫生健康委科学技术基金项目(gzwkj2021-103)