维生素E对离心运动后大鼠骨骼肌线粒体内丙二醛、超氧化物歧化酶的影响

Vitamin E effects on the malondialdehyde concentration and superoxide dismutase in skeletal muscle mitochondria following eccentric exercise in rats

背景：许多实验表明自由基的增加与骨骼肌运动性损伤有关,而维生素E作为一种抗氧化剂,具有清除自由基的功效,可减轻运动中抗氧化酶所受的自由基损伤,减缓疲劳出现,进而提高运动能力。目的：从细胞线粒体自由基代谢的角度,探讨维生素E对离心运动后大鼠骨骼肌细胞线粒体丙二醛、超氧化物歧化酶的影响,以进一步阐明维生素E抗骨骼肌运动性损伤的内在机制。设计、时间及地点：随机分组,动物实验观察,于2007-05/10在沈阳体育学院国家体育总局重点实验室和中国医科大学重点实验室完成。材料：雄性SD大鼠48只,体质量（304±12）g。随机分为对照组、运动组、生理盐水组、维生素E组,12只/组。方法：维生素E组腹腔注射维生素E胶丸,1.0~1.2mg/kg,总量为4mL/kg,初次注射时间为鼠正式实验前1d,以后每8h注射1次,共4次。生理盐水组以生理盐水为对照,注射方式、注射量及运动方式、处死时间同维生素E组。运动组只进行运动,不给予药物或生理盐水,对照组仅为常规饲养,无任何干预。采用一次力竭性下坡跑运动建造大鼠损伤模型,运动结束后,取大鼠右侧肱三头肌。主要观察指标：采用微量测定试剂盒和6010紫外-可见分光光度计测定丙二醛含量及超氧化物歧化酶活力。结果：肱三头肌细胞线粒体各组丙二醛、超氧化物歧化酶在离心运动后24h均显著增加（P〈0.01）。与运动组比较,生理盐水组丙二醛、超氧化物歧化酶值均无显著性差异（P〉0.05）,维生素E组丙二醛显著降低（P〈0.01）,而超氧化物歧化酶显著增高（P〈0.01）。结论：补充维生素E可降低骨骼肌细胞线粒体丙二醛的含量,增加细胞线粒体超氧化物歧化酶的活性,提高骨骼肌细胞的抗氧化能力,进而可减轻自由基对肌肉的损伤作用。维生素E对运动性骨骼肌损伤的预防作用主要是通过维生素E的抗氧化作用完成的。

BACKGROUND： It has been shown to exhibit the increase of free radical has relationship with exercise-induced skeletal muscle injury. As a kind of antioxidant, vitamin E has the ability of removing radicals, which can relieve antioxidase damage, and delay fatigue, eventually, improve the motor ability. OBJECTIVE： From the angle of free radical metabolism, to explore the effect of vitamin E on malondialdehyde （MDA） and superoxide dismutase （SOD） of mitochondria in skeletal muscular cell after eccentric exercise, additionally, to clarity the mechanism of vitamin E on reducing the skeletal muscle damage. DESIGN, TIME AND SETTING： The randomized grouping experiment of animal was carried out in the Key Laboratory of General Administration of Sport of China in Shenyang Sport University and the Key Laboratory of China Medical University from May to October in 2007. MATERIALS： A total of 48 male, Sprague Dawley rats, weighing （304±12） g were randomly divided into the of control, sport, physiological saline, and vitamin E groups, with 12 animals in each group. METHODS： Rats in the vitamin E group was administered （i.p.） 1 1.2 mg/kg vitamin E capsules once per eight hours, four times one day before experiment, and the amount of injecting volume was 4 mL/kg. The rats in physiological saline were injected by physiological saline, with the same injection methods of the vitamin E group. The models of injury were established by a bout of exhaustive eccentric exercise on a treadmill. After exercise, triceps brachiies were moved from the right side of rats. MAIN OUTCOME MEASURES： The content of MDA and activity of SOD were measured with the reagent-boxes and 6010 UV-seen spectrophotometer. RESULTS： The values of MDA, SOD of mitochondria in triceps brachiies cells in each group were greatly increased after 24 hour eccentric exercise （P 〈 0.01）. Compared with the sport group, the MDA content and SOD activity of the physiological saline group had no significantly difference （P 〉 0.05）, the value of MDA in the vitamin E group was greatly decreased （P 〈 0.01 ）, but activity of SOD was notably increased （P 〈 0.01）. CONCLUSIONS： Supplying of vitamin E could decrease the content of MDA in skeletal muscle mitochondria, increase the activity of SOD, and enhance the function of antiperoxidation in skeletal muscle, which can further relieve the effect of free radical on athletic injury. The preventive functions of vitamin E on anti-exercise-induced skeletal muscle injury were realized by its antioxidation effect.