利拉鲁肽基于线粒体-细胞色素C介导心肌细胞凋亡
Liraglutide ameliorates hypoxia/reoxygenation-induced H9C2 cardiomyocyte apop-tosis via mitochondrial-cytochrome C pathway
黄学明 1戴萌 2徐菁慧3
作者信息
- 1. 华北医疗集团总医院心内科,邯郸 056200
- 2. 华北油田总医院心内科,沧州 062550
- 3. 沧州市人民医院心内科,沧州 061000
- 折叠
摘要
目的 探讨利拉鲁肽在缺氧/复氧(hypoxia/reoxygenation,H/R)处理的心肌细胞中的作用及其潜在机制.方法 建立大鼠心肌细胞株(H9C2)H/R模型以模拟体外心肌缺血再灌注(ischemia/reperfusion,I/R)损伤.用四甲基偶氮唑盐[3-(4,5)-dimeth-ylthiahiazo(-z-y 1)-3,5-di-phenytetrazoliumromide,MTT]和 Annexin V FITC-PI 染色法测定细胞增殖和凋亡.检测细胞氧化应激产物和线粒体功能.用蛋白印迹法(Western blotting)检测细胞凋亡蛋白表达和细胞色素C的释放.结果 利拉鲁肽保护H9C2细胞免受H/R诱导的损伤,因其可减弱H/R对H9C2细胞活力、细胞凋亡和活性氧(reactive oxygen species,ROS)产生的影响(P<0.05).利拉鲁肽可保护线粒体功能并防止H/R损伤后H9C2细胞中细胞色素C的释放(P<0.05).结论 阐明了利拉鲁肽在治疗I/R相关心肌损伤中的潜在心血管保护作用.
Abstract
Objective To further study the role of liraglutide in cardiomyocytes treated with hypoxia/reoxygenation(H/R)and its underly-ing mechanism.Methods A H/R model of rat myocardial cell line(H9C2)was established to simulate myocardial ischemia/reperfusion(1/R)injury in vitro.3-(4,5)-dimethylthiahiazo(-z-y1)-3,5-di-phenytetrazoliumromide(MTT)and Annexin V FITC-PI staining methods were used to measure the cell proliferation and apoptosis.Cellular oxidative stress products and mitochondrial function were detected.West-em blotting was used to detect the expression of apoptosis-related protein and the release of cytochrome C.Results Liraglutide protected H9C2 cells from H/R-induced damage,because the administration of liraglutide attenuated the effects of H/R on H9C2 cell viability,apop-tosis and reactive oxygen species(ROS)production(P<0.05).More importantly,liraglutide protected mitochondrial function and prevented the release of cytochrome C in H9C2 cells after H/R injury(P<0.05).Conclusion These results revealed the potential cardio-vascular protective effects of liraglutide in the treatment of I/R-related myocardial injury.
关键词
利拉鲁肽/缺氧/复氧/线粒体-细胞色素C/心肌细胞株/凋亡Key words
liraglutide/hypoxia/reoxygenation/mitochondria-cytochrome C/H9C2/apoptosis引用本文复制引用
基金项目
河北省卫生健康委立项项目(2021)(20211484)
出版年
2024