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为了探讨急性运动所致疲劳的机理以及胆红素的保护作用 ,以大鼠急性运动为模型 ,对运动过程中线粒体的脂质过氧化、抗氧化酶活性的改变以及胆红素的保护作用进行了观察 ,结果显示 :急性运动后即刻 ,大鼠线粒体MDA含量、GSH -Px活性明显高于对照组 ,恢复 12小时后MDA含量、GSH -Px活性基本恢复 ;总SOD、Mn -SOD、Cu -Zn -SOD酶活性在运动后即刻有下降的趋势 ,运动后 12小时基本恢复。胆红素处理运动组与胆红素处理运动恢复组的这些指标与对照组基本接近。结果提示 :胆红素可以通过抑制线粒体的脂质过氧化 ,提高总SOD、Mn -SOD、Cu -Zn-SOD活性等途径来保护急性运动对骨骼肌线粒体的损伤
In order to investigate the mechanism of fatigue induced by acute exercise and the protective effect of bilirubin, the model of acute exercise in rats was used to model mitochondrial lipid peroxidation, changes of antioxidant enzyme activity and the protective effect of bilirubin during exercise The results showed that the content of MDA and the activity of GSH-Px in mitochondria were significantly higher than those in the control group immediately after acute exercise, and the content of MDA and the activity of GSH-PX recovered after 12 hours of recovery. The activities of total SOD, Mn -SOD and Cu - Zn-SOD activity decreased immediately after exercise, and basically recovered after 12 hours of exercise. These indexes of bilirubin group and bilirubin group were similar to those of control group. The results suggest that bilirubin can protect mitochondria from acute exercise by inhibiting the lipid peroxidation of mitochondria and increasing the activity of total SOD, Mn-SOD and Cu-Zn-SOD