运动性心肌微损伤发生中凋亡基因表达谱研究

The Expression of Apoptosis Gene in Injured Myocytes of Rats Induced by Exhausted Exercise

目的:对一次力竭运动后不同时间心肌凋亡基因表达谱进行研究,探讨其在运动性心肌微损伤发生中的可能作用与功能意义。方法:健康雄性SD大鼠50只,分为一次力竭游泳运动组(n=40)和对照组(n=10),一次力竭运动后,分不同时相取材,采用基因芯片技术对相关凋亡基因表达谱的进行分析。结果:一次力竭游泳运动后心肌细胞凋亡基因主要包括诱导凋亡基因(Bok、Bnip3)和调控凋亡的转录因子(Nfkbia、Sphk1、ATF-3以及Casp2)等两类凋亡基因的表达。其中,Bok、Nfkbia、Sphk1、ATF-3在一次性力竭运动后即刻出现显著性上调表达,且Bok在12小时又出现显著性上调表达。心肌促凋亡基因(Bnip3、Casp2)在运动后即刻出现显著性下调表达,且Bnip3在12小时又出现显著性下调表达。结论:(1)一次性力竭运动后,心肌促凋亡基因Bok、转录因子Nfkbia显著性上调表达,加速运动性心肌细胞凋亡的发生,可能参与运动性心肌微损伤发生过程的调节,构成了运动性心肌微损伤发生的重要机制。(2)一次性力竭运动后,心肌促凋亡基因Bnip3、Casp2显著性下调表达,细胞凋亡调控基因Atf3、Sphk1显著性上调表达,抑制心肌细胞凋亡的发生与发展,可能对运动心肌有保护作用,防止严重性心肌损伤的发生。

Objective To screen the myocardial apoptosis gene and observe its function in injured myocytes after single bout of exhausted exercise. Methods Fifty male Sprague-Dawley rats were randomly divided into sedentary control group and single bout of exhausted exercise group. Rats were killed at Oh, 6h, 12h, and 24h after exhausted exercise, and gene chip technology was applied to screen the myocardial apoptosis gene. Results Myocardial apoptosis gene mainly involved in Bok, Bnip3, Nfkbia, Sphkl, ATF-3, and Casp2 after the acute exhausted exercise. The expression of Bok, Nfkbia, Sphkl and ATF-3 at Oh after exhausted exercise was greatly upregulated, especially the expression of Bok at 12h after exercise was upregulated again. The expression of Bnip3 and Casp2 was greatly downregulated at Oh after exercise, especially the expression of Bnip3 at 6h after exercise was downregulated again. Conclusions （1） After single bout of exhausted exercise, the gene expression of Bok and Nfkbia was significantly upregulated, quickening the process of myocytes apoptosis and eventually leading to myocardial microinjury. （2） After single bout of exhausted exercise, the upregulated expression of Bnip3 and Casp2 and downregulated ATF-3 and Sphkl restrain the occurrence and/or development of myocytes apoptosis, and thus protect the myocytes from further severe injury.