辅酶NADH对运动疲劳小鼠心肌细胞损伤的保护作用  

Protective Effects of NADH on Cardiac Injury Induced by Excessive Exercise

作　　者：李萍[1] 唐念[2] 李艳琴[3] 

机构地区：[1]武汉体育学院武术学院,湖北武汉430079 [2]湖州师范学院体育学院,浙江湖州313000 [3]武汉大学药学院,湖北武汉430071

出　　处：《武汉体育学院学报》2012年第4期97-100,共4页Journal of Wuhan Sports University

基　　金：国家自然科学基金项目(81000574)

摘　　要：目的:探讨辅酶还原型烟酰胺腺嘌呤二核苷酸(reduced nicotinamide adenine dinucleotide,NADH)对运动疲劳所致小鼠心肌细胞损伤的保护作用及机制。方法:选取32只雄性昆明小鼠,随机分成4组:对照组、运动疲劳组、NADH正常对照处理组和运动疲劳NADH预处理组。采用反复力竭递增负荷跑台运动建立小鼠运动疲劳模型;分组处理后测定心肌组织超氧化物岐化酶(SOD)活性和丙二醛(MDA)含量;Rodamine123荧光染色后流式细胞仪检测细胞内线粒体膜电位的变化;AnnexinⅤ/PI双染流式细胞仪检测细胞凋亡率和坏死率。结果:NADH预处理组心肌组织超氧化物岐化酶(SOD)活性和丙二醛(MDA)含量较运动损伤组明显改善,细胞内线粒体膜电位增高,细胞凋亡率和坏死率降低。结论:NADH可减少运动疲劳所致氧化应激引起的心肌细胞损伤,可通过提高细胞线粒体功能起到保护的作用。The objective of this study was to explore the protection effects of NADH on Cardiac injury Induced by ex cessive exercise in vivo.Kunmin mice were divided four groups：control group and cardiac injury group,NADH con trol group,pretreatment with NADH before excessive exercise group.After the excessive exercise session,effect of NADH on the mice body weight,SOD activation and MDA level,the mitochondria membrane potential and the rate of apoptosis and necrosis were studied.It revealed that excessive exercises could induce SOD activation and MDA level increase.Mitochondria membrane potential decreased.The rate of apoptosis and necrosis increased.NADH could decrease SOD activation and MDA level,increase mitochondria membrane potential,and decrease the rate of apoptosis and necrosis induced by excessive exercise cardiac injury.The results showed that NADH pretreatment could reduce the oxidative injury and apoptosis induced by excessive exercise.

关 键 词：运动疲劳 NADH 心肌损伤 力竭运动 

分 类 号：G804.7[文化科学—运动人体科学]