力竭运动性猝死模型大鼠运动皮质Bax、Bcl-2及脑源性神经营养因子的表达变化

Expression levels of Bax, Bcl-2 and brain-derived neurotrophic factor in the rat brain motor cortex after over fatigue-induced sudden death

背景:运动性猝死是运动实践中的常见现象,因偶发故其机制不明。目的:观察运动性猝死大鼠的运动皮质细胞形态学改变、凋亡调控因子Bax、Bcl-2及脑源性神经营养因子的表达变化,探讨连续力竭性负重游泳训练中运动性猝死的发生及调控机制。方法:130只雄性SD大鼠随机选7只为空白对照组,其余大鼠在疲劳造模后按36 h的训练周期、对大鼠进行连续力竭性负重游泳训练,并分别在6×36 h、9×36 h与12×36 h训练后随机处死7只大鼠分别记为连续力竭性负重游泳训练1,2,3组(力竭运动1,2,3组);将多次相同模型实验中、6×36 h后偶然出现在每次训练中或训练后24 h内的死亡大鼠(排除因呛水死亡)记为运动性猝死组(n=5)。采用苏木精-伊红染色观察大脑运动皮质细胞的形态结构变化,免疫组织化学染色检测Bax、Bcl-2蛋白及脑源性神经营养因子的阳性表达变化。结果与结论:(1)与空白对照组相比,力竭运动1,2,3组和运动性猝死组的运动皮质细胞形态结构发生明显改变,Bax、Bcl-2蛋白及脑源性神经营养因子的阳性表达率明显增高(P<0.05);(2)在力竭运动1,2,3组和运动性猝死组中Bax及Bcl-2蛋白呈递增趋势,Bcl-2蛋白表达增强程度高于Bax蛋白;而脑源性神经营养因子的表达呈先增加后降低的趋势;(3)结果表明,力竭运动组及运动性猝死组中运动皮质细胞内Bax、Bcl-2蛋白及脑源性神经营养因子的阳性表达的增强可能与运动皮质细胞的保护抑制机制有关;过度疲劳时运动皮质内脑源性神经营养因子表达的下降可能是诱发运动性猝死的原因之一。

BACKGROUND： Exercise-induced sudden death is a common phenomenon during exercising, but the mechanism is not fully understood. OBJECTIVE： To investigate the morphological changes of motor cortex and the expression levels of Bax, Bcl-2 and brain-derived neurotrophic factor（BDNF）, and to explore the occurrence and regulatory mechanism of exercise-induced sudden death during the training of continuously exhaustive loaded-swimming. METHODS： Seven selected from 130 male Sprague-Dawley rats were randomly as blank control group and the remaining rats were modeled into over fatigue, followed by continuously exhaustive loaded-swimming with the training cycle of 36 hours. Then seven rats were killed as groups 1, 2 and 3 at 6, 9, 12 and 36 hours of exhaustive loaded-swimming and all dead rats in near several experiments in the same model without choking water in each training or within 24 hours after the 6th 36 hours of training as exercise-induced sudden death group（n=5）. The morphological changes of motor cortex were observed by hematoxylin-eosin staining, and the expression levels of Bax and Bcl-2 proteins and BDNF were examined by immunohistochemistry. RESULTS AND CONCLUSION：（1） Compared with the blank control group, the morphology of motro cortex changed significantly, and the expression levels of Bax and Bcl-2 proteins and BDNF in the groups 1, 2, and 3 and exercise-induced sudden death group were significantly up-regulated（P 〈0.05）.（2） Moreover, in the groups 1, 2, and 3 and exercise-induced sudden death group, the expression levels of Bax and Bcl-2 proteins showed an increasing trend, especially Bcl-2; while, the expression level of BDNF increased firstly and then decreased.（3） In conclusion, the enhanced expression levels of Bax and Bcl-2 proteins and BDNF in brain motor cortex of fatigue and exercise-induced sudden death groups maybe related to the protection-inhibition mechanism. The reduced expression of BDNF in brain motor cortex may be one of the reasons inducing sudden death during over fatigue.