川芎嗪干预静态姿势负荷模型大鼠不同时相自由基及酶代谢的变化.

BACKGROUND: Ligustrazine has been shown to protect the rat skeletal muscle under state of disuse, and protect against skeletal muscle atrophy in denervated rats. OBJECTIVE: To investigate the effects of ligustrazine on different phases of free radicals and enzyme metabolism after static postural load in rats. METHODS: The study was approved by the Laboratory Animal Ethical Committee of Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology. Thirty-six SPF male Sprague-Dawley rats were randomized into control, model and ligustrazine groups. At 0.5 hour before experiment, the rats in the control and model groups were given 2 mL solvent via gavage, and ligustrazine group was given 2 mL ligustrazine solution. During the experiment, the rats in the control group received no load. The rats in the model and ligustrazine groups were fixed with the splint to maintain the static posture load, and the trunk part was fixed in the pre-made wooden box to maintain the straight state for 10 hours, to establish a static posture load rat model. The serum level of malonaldehyde, serum lactic dehydrogenase activity and Ca2+-ATPase activity in the soleus at different phases (2,5,8 and 10 hours) were detected. RESULTS AND CONCLUSION: (1) The serum level of malonaldehyde, serum lactic dehydrogenase activity and Ca2+-ATPase activity in the soleus did not change with time in the control group. Compared with 2 hours, in the model group, the serum level of malonaldehyde and serum lactic dehydrogenase activity were increased, and the Ca2+-ATPase activity was significantly decreased at 5, 8 and 10 hours (P < 0.05 or P < 0.01). Compared with 2 hours, in the ligustrazine group, the serum level of malonaldehyde and serum lactic dehydrogenase activity were decreased, and the Ca2+-ATPase activity was significantly increased at 5, 8 and 10 hours (P < 0.05 or P < 0.01). Compared with the control group at the same phase, the serum level of malonaldehyde and serum lactic dehydrogenase activity in the model group were increased, and the Ca2+-ATPase activity was significantly decreased (P < 0.01). Compared with the model group at the same phase (except 2 hours), the serum level of malonaldehyde and serum lactic dehydrogenase activity were significantly decreased in the ligustrazine group, and the Ca2+-ATPase activity was significantly increased (P < 0.01). (2) These results indicate that ligustrazine can significantly reduce the serum malonaldehyde content and serum lactic dehydrogenase activity caused by static postural load at different phases, and significantly increase the Ca2+-ATPase activity in the soleus, so as to alleviate the body injury caused by long-term static postural load. [ABSTRACT FROM AUTHOR]