力竭运动致大鼠心肌组织损伤后p53蛋白表达变化

来源 :中国职业医学 | 被引量 : 0次 | 上传用户:winxb
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目的观察p53蛋白在力竭运动损伤大鼠心肌组织中的表达变化。方法 Wistar大鼠12只,随机分为对照(C)组和力竭运动损伤(EI)组。EI组大鼠进行梯度负荷的跑台运动至力竭,共训练10 d;取血测定丙二醛(MDA)水平及超氧化物歧化酶(SOD)活力等;用光镜和电镜对心肌进行组织学观察;采用Western-blot和免疫组织化学法检测p53蛋白表达。结果力竭运动后,大鼠血液中乳酸脱氢酶(LDH)活力升高;一氧化氮(NO)水平降低;MDA水平升高;同时SOD活力下降。心肌组织苏木素-伊红染色法染色可见,大鼠心肌和血管内皮细胞空泡变性和心肌间质水肿等;电镜可见,血管内皮细胞发生典型细胞凋亡特征。Western-blot结果表明,C组心肌组织中p53蛋白仅极少量表达,而EI组心肌中p53蛋白表达水平升高;免疫组织化学结果显示,与C组比较,EI组心肌中p53蛋白表达升高,且在心肌和内皮细胞中均有表达。结论力竭运动不仅可致心肌氧化应激损伤,还可诱发大鼠心血管内皮细胞凋亡。p53蛋白在力竭运动损伤心肌组织中表达升高。 Objective To observe the expression of p53 protein in myocardial tissue after exhaustive exercise. Methods Twelve Wistar rats were randomly divided into control group (C) and exhaustive exercise injury (EI) group. EI rats were subjected to gradient load treadmill exercise to exhaustion for a total of 10 days. Blood samples were collected for determination of malondialdehyde (MDA) and superoxide dismutase (SOD) activity. Myocardium was examined by light and electron microscopy Histological observation; p53 protein expression was detected by Western-blot and immunohistochemistry. Results After exhaustive exercise, lactate dehydrogenase (LDH) activity in the blood of rats increased; nitric oxide (NO) level decreased; MDA level increased; at the same time, SOD activity decreased. Myocardial tissue hematoxylin-eosin staining staining, myocardial and endothelial cell vacuolar degeneration and myocardial interstitial edema, etc .; electron microscopy, endothelial cells typical apoptotic characteristics. The results of Western-blot showed that the expression of p53 protein in myocardium of EI group was very little, while the expression of p53 protein in EI group was increased. Immunohistochemistry showed that the expression of p53 protein in EI group was higher than that in group C , And expressed in both myocardium and endothelial cells. Conclusion Exhaustion can not only induce myocardial oxidative stress injury, but also induce apoptosis of rat cardiovascular endothelial cells. p53 protein in exhaustive exercise-induced myocardial tissue increased expression.
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