一次性力竭运动模型大鼠心肌氧化损伤的作用途径  

Mechanism of myocardial oxidative damage in a rat model of one-time exhaustive exercise

作　　者：谢文杰 周刚[1] 谢金美 刘姣 李鹏飞 扬帆 崔迪 Xie Wenjie;Zhou Gang;Xie Jinmei;Liu Jiao;Li Pengfei;Yang Fan;Cui Di(School of Physical Education,Hunan University,Changsha 410000,Hunan Province,China;Zhumadian Municipal First People’s Hospital,Zhumadian 463100,Henan Province,China)

机构地区：[1]湖南大学体育学院,湖南省长沙市410000 [2]驻马店市第一人民医院,河南省驻马店市463100

出　　处：《中国组织工程研究》2021年第2期247-252,共6页Chinese Journal of Tissue Engineering Research

基　　金：湖南省自然科学基金项目(12JJ3093),项目负责人:周刚。

摘　　要：背景:力竭运动是生物体在超出其生理极限下进行的剧烈身体活动,它会引起机体各组织产生一系列的变化。心肌运动性氧化应激损伤是指生物体在力竭运动下,通过氧化应激信号途径产生自由基,并对心肌细胞产生损伤的现象。目的:基于PKC-NOX-ROS途径下,探讨一次性力竭运动造成大鼠心肌运动性氧化应激损伤的机制。方法:成年雄性SD大鼠30只随机分为对照组、力竭运动组、力竭运动+药物组,每组10只。力竭运动+药物组连续3 d注射蛋白激酶C(PKC)抑制剂chelerythrine 5 mg/kg,力竭运动组、力竭运动+药物组大鼠以25 m/min的速度在0°坡度跑台上运动至力竭,对照组不做处理。运动后即刻取样,先进行采血,再取出左心室以苏木精-伊红染色,观察心肌细胞形态学变化;检测血清与心肌组织丙二醛、心肌活性氧(ROS)水平;大鼠心肌组织中PKC、NOX2、NOX4、3-NT的蛋白表达采用Western blotting法测定。结果与结论:①力竭运动组、力竭运动+药物组心肌组织均有损伤,且力竭运动+药物组与力竭运动组相比,心肌组织损伤显著降低;②与对照组相比,力竭运动组心肌组织中活性氧水平显著升高(P<0.05);③与对照组相比,力竭运动组、力竭运动+药物组心肌组织中丙二醛水平均显著升高(P<0.01),力竭运动组血清丙二醛浓度显著升高(P<0.05);④与对照组相比,力竭运动后力竭运动组大鼠心肌组织中PKC、NOX2、NOX4、3-NT的蛋白表达水平均显著增加(P<0.01);与力竭运动组相比,力竭运动+药物组大鼠心肌组织中NOX2、NOX4显著下降(P<0.01),3-NT显著下降(P<0.05);⑤提示一次性力竭运动可激活大鼠心肌细胞内PKC并增加其蛋白表达,进而诱导心肌内NOX2与NOX4蛋白表达增加,催化活性氧大量生成,并导致过氧亚硝酸阴离子过量生成,从而产生心肌氧化损伤。BACKGROUND:Exhaustive exercise is a vigorous physical activity performed by an organism beyond its physiological limits,and it causes a series of histological changes in the body.Myocardial exercise-induced oxidative stress injury means that the organism generates free radicals through oxidative stress signal pathway to damage myocardial cells under exhaustive exercise.OBJECTIVE:To explore the mechanism of oxidative stress injury in rat myocardium caused by one-time exhaustive exercise based on the protein kinase C(PKC)/NOX pathway.METHODS:Thirty adult male Sprague-Dawley rats were randomly divided into a control group,an exhaustive exercise group,and an exhaustive exercise+drug group,with 10 rats in each group.The exhaustive exercise+drug group was injected with PKC inhibitor chelerythrine(5 mg/kg body weight)for 3 consecutive days.Rats in the two exercise groups exercised at a speed of 25 m/min on a 0°incline treadmill until exhaustion.Immediately after exercise,blood sample was collected from each rat,and then the rat’s left ventricle was removed for hematoxylin-eosin staining to observe the morphological changes of myocardial cells.Serum and myocardial malondialdehyde and myocardial reactive oxygen species levels were detected.The protein expressions of PKC,NOX2,NOX4 and 3-NT in rat myocardial tissue were determined by western blot.RESULTS AND CONCLUSION:The myocardial tissues in the exhaustive exercise and exhaustive exercise+drug groups were damaged,but the damage was significantly eased in the exhaustive exercise+drug group compared with the exhaustive exercise group.Compared with the control group,the reactive oxygen species level in the myocardial tissue of the exhaustive exercise group increased significantly(P<0.05).Compared with the control group,the content of malondialdehyde in the myocardial tissues of the exhaustive exercise and exhaustive exercise+drug groups was significantly increased(P<0.01),and the concentration of serum malondialdehyde in the exhaustive exercise group was significantly in

关 键 词：力竭运动 心肌 氧化损伤 应激 活性氧 丙二醛 动物 模型 

分 类 号：R459.9[医药卫生—治疗学] R318[医药卫生—临床医学]