摘要
目的:研究长期力竭性训练对大鼠海马神经元凋亡的影响及其基因调控机制;方法:对大鼠进行为期8周的力竭性游泳训练,用DNA原位末端标记法检测海马神经元的凋亡,并用免疫组化的方法观察海马神经元中bcl-2、bax的免疫反应活性;结果:1)长期力竭性训练后,大鼠海马神经元凋亡显著增加。海马神经元凋亡可能是力竭性训练导致运动能力降低和中枢性运动疲劳的病理生理机制。2)长期力竭性训练后,大鼠海马神经元中bcl-2蛋白的表达显著下降,bax蛋白的表达显著增加。因此,力竭性训练可抑制海马神经元bcl-2蛋白的表达而促进bax蛋白的表达,这可能是力竭性训练导致大鼠海马神经元凋亡发生的基因调控机制。
To Study the effects of long-term exhaustive training on the death of rats' hippocampus nerve cell, rats make eight weeks exhaustive swimming training. The death of rats' hippocampus nerve cell is signaled with DNA end method. The immune ability of bcl-2 and bax in hippoeampus is observed with the method of immune group. After long-term exhaustive training, the death of rats' hippocampus nerve cell increases, so the death may be the cause of low sporting capability and sports fatigue. After long-term exhaustive training, bcl-2 protein expression in hippocampus decreases obviously while bax protein expression increases greatly. Therefore, exhaustive training may be the cause of restricting bcl-2 and promoting bax, which may be the gene control system of the death of rats' hippocampus nerve cell.
出处
《北京体育大学学报》
CSSCI
北大核心
2007年第8期1060-1062,共3页
Journal of Beijing Sport University