摘要
为了研究过度训练对大鼠心肌细胞凋亡的影响 ,通过对大鼠进行力竭性游泳训练建立大鼠过度训练模型 ,用DNA原位末端标记法检测心肌细胞的凋亡 ,并用免疫组化的方法检测心肌细胞中bcl- 2和Fas蛋白的表达情况。结果发现 :①过度训练时 ,大鼠心肌细胞凋亡显著增加。心肌细胞凋亡可能是过度训练影响心血管功能的病理生理机制。②过度训练时 ,大鼠心肌细胞中bcl- 2蛋白的表达显著下降 ,Fas蛋白的表达轻度增加。因此 ,过度训练抑制bcl- 2蛋白的表达而促进Fas蛋白的表达 ,这可能是过度训练时大鼠心肌细胞凋亡发生的基因调控机制。③过度训练时 ,大鼠心肌组织和血清中SOD活性显著下降 ,MDA含量显著增加。因此 ,过度训练时机体抗氧化能力下降 ,导致氧自由基生成增多。这可能也是心肌细胞凋亡的调节机制。
In order to investigate the effects of overload training on apoptosis of cardiac muscle cell in rats,overtraining model was established based on exhaustive swimming training.The apoptotic myonuclei were detected by terminal deoxynucleotidyl transferase-mediated end-labeling of DNA in nuclei in tissue sections,and the expression of bcl-2 protein and Fas protein were detected by immunohistochemistry. Results ①the apoptotic myonuclei of cardiac muscle cell increased significantly after overload training.The increase of apoptosis of cardiomyocyte might be the pathophysiological mechanism for lowering cardiovascular function.②The expression of bcl-2 protein decreased significantly and the expression of Fas protein increased softly in cardiac muscle cell after overtraining.Therefore,the overtraining could inhibit the expression of bcl-2 protein and enhance the expression of Fas protein,which might be the mechanism of genetic controls on apoptosis in cardiac muscle cell.③After overload training,the SOD activity decreased and the MDA content increased significantly in cardiac muscles and in serum.Therefore,overtraining could cause the decrease of the capacity of antioxidation and cause the increase of oxygen free radicals,which might be the mechanism for regulating the apoptosis of cardiac muscle cell.
出处
《中国运动医学杂志》
CAS
CSCD
北大核心
2000年第4期356-359,共4页
Chinese Journal of Sports Medicine