附子多糖对力竭运动小鼠心肌过氧化损伤的保护作用

目的通过建立灌服附子多糖小鼠力竭性游泳实验模型,观察小鼠心肌自由基代谢和细胞凋亡的变化,探讨附子多糖(Fuzi Polysaccharide,FPS)对运动过程中心肌过氧化损伤的保护作用。方法雄性昆明小鼠随机分成安静组、力竭组、力竭 VitC对照组、力竭 附子多糖组,采用一次性力竭游泳建立模型。观察小鼠游泳耐力,测定心肌组织超氧化物歧化酶(Superoxide Dismutase,SOD)、过氧化氢酶(Catalase,CAT)、谷光甘肽过氧化物酶(Glutathione Peroxidase,GSH-Px)的活性以及丙二醛(Malondialdehyde,MDA)的含量;用Hoechst荧光染色法观察凋亡细胞核并计算凋亡指数,并检测心肌组织Bcl-2和Caspase-3的基因表达情况。结果附子多糖能够显著提高力竭小鼠的心肌SOD、CAT、GSH-Px活性,降低MDA含量;降低心肌细胞凋亡指数,增强Bcl-2的表达,抑制Caspase-3的表达降低,提高运动耐力。结论附子多糖能够通过其抗氧化作用及影响相关凋亡基因的表达,发挥抗过氧化损伤的作用,增强运动能力。

Effects of fuzi polysaccharide on myocardium injury of peroxidization induced by exhaustive exercise in mice

Objective To observe the effects of Fuzi polysaccharice(FPS) against mice cardiomyocyte injury of peroxidation induced by exhaustive swimming. Methods Male kumming mice were set up animal model by exhaustive swimming. Mice were randomly divided into an sedentary condition, exhaustive exercise only, exhaustive exercise with administration of FPS(FPS) and Vitamin C(VitC) groups. The swimming endurance was determined except sedentary group. The activity of superoxide dismutase(SOD), catalase(CAT), glutathione qeroxidase(GSH-Px) and the content of malondialdehyde(MDA) in myocardium were measured. At the same time cell apoptosis index was counted by fluorescence staining of hoechst33258 and Bcl-2, caspase-3 genes expression were investigated. Results The activity of SOD, CAT and GSH-Px was significantly increased and the content of MDA was decreased with administration of FPS.Cardiomyocyte apoptosis index also significantly lowered. At the same time Bcl-2 gene expression was upregulated and caspase-3 gene expression was remarkably inhibited. Conclusion FPS can prevent cardiomyocyte injury of peroxidization induced by exhaustive swimming via it's antioxidation and regulation effects on the expression of Bcl-2 and Caspase-3.