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[Protective effects of salidroside on oxidative damage in fatigue mice]
Li Ma1, Dong-lian Cai, Huai-xing Li
1Department of Clinical Nutrition, Changzheng Hospital, Second Military Medical University, Shanghai 200003, China. mali106@126.com
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 auto-biochemistry analyzer. The activities of superoxide dismutase (SOD), glutathione 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.