T3对缺氧/复氧致小鼠心肌细胞凋亡的影响  

Effects of T3 on Hypoxia/reoxygenation-induced Apoptosis Inmouse Cardiomyocytes

作　　者：廖小婷 曾彬[1] 刘磊[1] Liao Xiaoting;Zeng Bin;Liu Lei(Department of Cardiology,Renmin Hospital of Wuhan University,Cardiovascular Research Institute,Wuhan University,Hubei Key Laboratory of Cardiology,Hubei 430060,China)

机构地区：[1]武汉大学人民医院心内科、武汉大学心血管病研究所、心血管病湖北省重点实验室

出　　处：《医学研究杂志》2019年第11期19-23,30,共6页Journal of Medical Research

基　　金：国家自然科学基金资助项目(81570333)

摘　　要：目的探讨小鼠乳鼠心肌细胞在缺氧和缺氧/复氧下心肌细胞损伤及凋亡情况及T3对心肌细胞缺氧/复氧损伤的影响.方法采用1~2天新生昆明小鼠,分离培养心室肌细胞,分别给予不同时间缺氧及缺氧/复氧处理,观察细胞状态及细胞搏动次数,流式细胞仪分析细胞凋亡;给予T3预处理后进行缺氧/复氧损伤,流式细胞仪检测细胞凋亡,JC-1染色检测细胞线粒体膜电位;应用Western blot法检测心肌细胞凋亡蛋白.结果缺氧可造成心肌细胞凋亡,缺氧时间越长,心肌细胞损伤越重,缺氧/复氧可进一步加重心肌细胞损伤,增加细胞凋亡率;T3预处理可减少缺氧/复氧所致损伤,减少细胞凋亡率,降低凋亡蛋白caspase-3、Bax的表达,减少细胞线粒体膜电位损伤.结论缺氧可诱导心肌细胞损伤,缺氧时间越长,心肌细胞损伤越重,且缺氧/复氧损伤对心肌细胞损害更大;T3预处理可以保护心肌细胞并减少细胞凋亡.Objective To investigate the damage of cardiomyocytes induced by hypoxia and hypoxia/reoxygenation in neonatal mice and the effect of T3 on hypoxia/reoxygenation injury of cardiomyocytes.Methods Ventricular myocytes were isolated and cultured from 1-2 day old Kunming mice,and treated with hypoxia at different time pointsand hypoxia/reoxygenation injury.The cell status and pulsation times were observed,and the apoptosis was analyzed by flow cytometry.Mitochondrial membrane potential was detected by JC-1 staining and Western blot was used to detect cardiomyocyte apoptosis protein Bax and caspase-3.Results Hypoxia could induce cardiomyocyte apoptosis,the apoptosis rate of cardiomyocytes was increased with the hypoxia time prolonging.Hypoxia/reoxygenation could further aggravate the injury of cardiomyocyte and increase the apoptosis rate.T3 pretreatment could reduce the injury caused by hypoxia/reoxygenation,decrease the cell apoptosis rate,the expression of apoptotic proteins caspase 3 and Bax were also decreased,and increased mitochondrial membrane potential of hypoxia/reoxygenation induced cardiomyocytes.Conclusion Hypoxia can induce cardiomyocyte injury,the injury was increased with hypoxia time prolonging,and hypoxia/reoxygenation induced injurywas more serious;T3 preconditioning can protect cardiomyocyte and reduce apoptosis.

关 键 词：心室肌细胞 缺氧/复氧损伤 细胞凋亡 线粒体膜电位 

分 类 号：R5.3[医药卫生—内科学]