红景天苷对疲劳小鼠氧化损伤的保护作用

Protective effects of salidroside on oxidative damage in fatigue mice

目的:探讨红景天苷对疲劳小鼠氧化损伤保护作用的机制。方法:32只昆明种雄性小鼠按体质量随机分为正常对照组、红景天苷组、运动组及红景天苷+运动组。红景天苷组及红景天苷+运动组小鼠予红景天苷180mg/(kg.d)灌胃给药,正常对照组及运动组予相同体积[0.02mL/(g.d)]蒸馏水灌胃,连续灌胃15d。末次给药后30min,运动组及红景天苷+运动组小鼠无负重游泳120min。游泳后立即取材,全自动生化仪检测血浆乳酸脱氢酶(lactate dehydrogenase,LDH)、肌酸激酶(creatine kinase,CK)及肌酸激酶同工酶MB(creatine kinase-myocardial band isoenzyme,CK-MB)活性;采用试剂盒检测肝组织匀浆中过氧化物歧化酶(superoxide dismutase,SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)活性和丙二醛(malondialdehyde,MDA)含量;电子显微镜观察心肌和骨骼肌超微结构变化。结果:与不运动比较,长时间运动可明显提高小鼠血浆LDH、CK、CK-MB活性(P<0.01,P<0.05),而红景天苷可降低小鼠血浆CK及CK-MB活性(P<0.05,P<0.01);红景天苷与长时间运动有交互作用,红景天苷可拮抗长时间运动导致的血浆LDH、CK及CK-MB活性升高(P<0.05)。与不运动比较,长时间运动可显著降低小鼠血浆SOD及GSH-Px活性(P<0.01),升高小鼠血浆MDA含量(P<0.01);红景天苷可明显升高小鼠血浆SOD及GSH-Px活性(P<0.01,P<0.05),显著降低小鼠血浆MDA含量(P<0.01);红景天苷可拮抗长时间运动导致的小鼠血浆SOD活性降低(P<0.05)。电子显微镜结果表明长时间耐力运动后骨骼肌和心肌出现明显的损伤,运动组小鼠骨骼肌及心肌超微结构损伤较红景天苷+运动组明显。结论:红景天苷对运动所导致的氧化损伤具有一定的保护作用。

Objective： To study the protective effects of salidroside on oxidative damage in fatigue mice. Methods： Thirty-two male Kunming mice were randomly divided into four groups based on body weight：normal control group, salidroside group, training group and salidroside plus training group. The mice in the normal control group and the training group were given distilled water and mice in the salidroside group and the salidroside plus training group were given 180 mg/（kg·d） salidroside for 15 days. At 30 min after the last administration, the mice in the training group and the salidroside plus training group were forced to swim for 120 min. Finally, all the mice were killed. The activities of lactate dehydrogenase （LDH）, creatine kinase （CK） and creatine kinase-myocardial band isoenzyme （CK-MB） in plasma were determined by an autobiochemistry analyzer. The activities of superoxide dismutase （SOD）, glutathion peroxidase （GSH-Px） and the content of malonaldehyde （MDA） in liver tissue were also detected. The changes of ultrastructures of the skeletal muscle and cardiac muscle were observed under an electron microscope. Results： Compared with no swimming, long-time swimming could significantly increase the activities of LDH, CK and CK-MB in plasma （P〈0.05, P〈0.01）, while salidroside could significantly decrease the activities of CK and CK-MB in plasma induced by long-time swimming （P〈0.05, P〈0.01）. There existed interactions in LDH, CK and CK-MB activities between salidroside and long-time swimming （P〈0.05）. Compared with no swimming, long-time swimming could significantly decrease the SOD and GSH-Px activities and increase the MDA content in liver tissue （P〈0.01）. Salidroside could significantly increase the GSH-Px and SOD activities and decrease the MDA content in liver tissue （P〈0.05, P〈0.01）. However, there were no interactions in GSH-Px activity and MDA content between salidroside and long-time swimming （P〈0.05）. After long-time swimming, more ultrastructural lesions were found in the cardiac muscle and skeletal muscle in the training group than in the salidroside plus training group. Conclusion： Salidroside may play a role in protecting the mice from oxidative damage caused by long-time endurance training.