NF-κB-p65、ICAM-1和细胞凋亡在力竭性运动诱发延迟性心肌损伤中的作用

Role of NF-κB-p65,ICAM-1 and apoptosis in exhausted exercise-induced delayed-onset myocardial injury

目的:观察反复力竭性游泳运动后,不同时相大鼠心肌组织中核转录因子-κB(NF-κB)-p65、细胞间黏附因子-1(ICAM-1)和细胞凋亡的动态变化,以评价在运动延迟性心肌损伤中的作用。方法:采用反复力竭性游泳运动建立延迟性心肌损伤大鼠模型。将无训练的80只Wistar雄性大鼠随机分为安静对照组和反复力竭性运动后即刻组、3 h组、6 h组、12 h组、24 h组、48 h组和96 h组。每组10只大鼠(n=10)。分别于末次运动后即刻、3、6、12、24、48 h和96 h快速取出心脏,应用免疫组化染色法和DNA原位末端标记(TUNEL)法检测大鼠心肌组织中NF-κB-p65和ICAM-1表达的水平和细胞凋亡的动态变化。结果:与安静对照组比较,反复力竭性运动后不同时相大鼠心肌细胞中NF-κB-p65和ICAM-1蛋白的表达及细胞凋亡指数均显著增加(分别为P<0.05和P<0.01),其中心肌细胞中NF-κB-p65的表达和细胞凋亡于运动后48 h达高峰,ICAM-1蛋白的表达于运动后即刻达高峰,运动后96 h有所减轻。结论:反复力竭性运动可以造成早期心肌缺血缺氧损伤,刺激心肌细胞中NF-κB-p65和ICAM-1表达的水平的升高,促进炎症反应,并诱导心肌细胞凋亡,进一步加重运动后早期心肌损伤,诱发延迟性心肌损伤。

AIM： To investigate the dynamic changes of nuclear transcription factor-kappa B （NF-KB） p65, intracellular adhesion molecule-1 （ICAM-1） and apoptosis in myocardium of rats at different time periods after repeated exhausted exercise and to explore their roles in the development of exercise-induced delayed-onset myocardial injury. METHODS ： The animal model of delayed-onset myocardial injury was established by repeated exhaustive swimming. Eighty male Wistar rats were divided randomly into seden- tary control group and exhausted exercise groups, namely, 3-, 6-, 12-, 24-, 48- and 96-h groups. Rat hearts were rapidly excised at respective time points of 3-, 6-, 12-, 24-, 48- and 96-h immediately after the exhausted exercise. The expressions of NF-KB-p65 and ICAM-1 proteins were detected by immuno- histochemical staining and apoptotic cells were assayed by TUNEL method. RESULTS： Compared with those rats in the sedentary control group, the expressions of NF-KB-p65 and ICAM-1 proteins and apoptosis indexes in rat myocardium significantly increased at different time periods after repeated exhaustive exercise （P 〈0. 05 and P 〈0. 01）. The expressions of NF-KB-p65 and apoptosis peaked at 48 h and ICAM-I proteins peaked at the time points immediately after exercise and decreased at 96 h post-exercise. CONCLUSION： The hypoxic-ischemic rat myocardial damage induced by repeated exhaustive exercise could lead to high expressions of NF,KB-p65 and ICAM-1, which promotes the inflammatory responses and apoptosis of myocytes and further aggravates early myocardial injury, resulting in exercise-induced delayed-onset myocardial injury.