中国组织工程研究

中国组织工程研究 ›› 2016, Vol. 20 ›› Issue (49): 7377-7383.doi: 10.3969/j.issn.2095-4344.2016.49.012

• 运动医学动物模型 Animal models of sports medicine • 上一篇    下一篇

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

阳仁均1，殷维瑶2，李  华3   

  1. 1成都体育学院运动医学系，四川省成都市  610041；2四川大学华西临床医学院，四川省成都市   610041；3四川大学华西基础医学与法医学院，四川省成都市  610041
  • 收稿日期:2016-09-04 出版日期:2016-11-30 发布日期:2016-11-30
  • 通讯作者: 李华，博士，教授，硕士生导师，四川大学华西基础医学与法医学院，四川省成都市 610041
  • 作者简介:阳仁均，男，1989年生，四川省大英县人，2016年成都体育学院毕业，硕士，主要从事运动性疲劳发生机制与消除手段的研究。
  • 基金资助:

    四川省科技计划项目(2014SZ0158)“高原-亚高原交替训练的实验研究-以甘孜中长跑运动员为例”

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

Yang Ren-jun1, Yin Wei-yao2, Li Hua3   

  1. 1Department of Sports Medicine, Chengdu Sport Institute, Chengdu 610041, Sichuan Province, China; 2West China School of Medicine/West China Hospital, Sichuan University, Chengdu 610041, Sichuan Province, China; 3West China College of Basic and Forensic Medicine, Sichuan University, Chengdu 610041, Sichuan Province, China
  • Received:2016-09-04 Online:2016-11-30 Published:2016-11-30
  • Contact: Li Hua, M.D., Professor, Master’s supervisor, West China College of Basic and Forensic Medicine, Sichuan University, Chengdu 610041, Sichuan Province, China
  • About author:Yang Ren-jun, Master, Department of Sports Medicine, Chengdu Sport Institute, Chengdu 610041, Sichuan Province, China
  • Supported by:

    the Science and Technology Program of Sichuan Province, No. 2014SZ0158

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摘要：

 

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文题释义：
运动性猝死：是运动员或体育锻炼者在运动中或运动后24 h内，有症状或无症状情况下的意外死亡，运动负荷是诱发运动性猝死的主要因素之一，并且猝死的危险性随负荷强度增高而增大，大强度运动下运动性猝死的发生机制尚不清楚，分析大强度运动下出现的运动性猝死案例有助于探索其发生机制。
脑源性神经营养因子：是主要在中枢神经系统内表达的具有神经营养作用的蛋白质，它是一种脑组织细胞保护因子，在海马体和脑皮质内含量最高。力竭运动时大脑的相对缺血缺氧诱导发生了两个相反的级联过程，一个是由基因表达调控的神经元细胞主动性的死亡过程；另一个则是受到损伤刺激的神经元通过上调脑源性神经营养因子的表达水平而产生的一种主动性的细胞保护过程，从而使细胞能够抵御运动性脑缺血缺氧引起的病理生理损伤而得以存活。

摘要
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。

中国组织工程研究杂志出版内容重点：肾移植；肝移植；移植；心脏移植；组织移植；皮肤移植；皮瓣移植；血管移植；器官移植；组织工程
ORCID: 0000-0001-5187-9404(阳仁均)

关键词: 实验动物, 运动系统动物模型, 运动性猝死, 运动皮质, Bcl-2, Bax, 脑源性神经营养因子, 调控

Abstract:

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.

中国组织工程研究杂志出版内容重点：肾移植；肝移植；移植；心脏移植；组织移植；皮肤移植；皮瓣移植；血管移植；器官移植；组织工程

Key words: Models, Animal, Death, Sudden, Motor Cortex, Brain-Derived Neurotrophic Factor, Tissue Engineering

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