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目的探讨褪黑素对锰致小鼠运动障碍及纹状体损伤的影响。方法小鼠84只,均分为6组,分别为对照组及低、中、高Mn组,褪黑素(MT)对照组和MT+高Mn组。第5、6组提前皮下注射给予5 mg/kg MT,2 h后,第2~4和6组分别腹腔注射给予12.5、25、50和50 mg/kg MnCl2,连续2周。观察小鼠的自主活动情况,检测纹状体GSH-Px、SOD和γ-GCS的活力、表达及蛋白水平。结果随着锰浓度的升高,自主活动和站立次数逐渐减少;纹状体γ-GCS、GSH-Px和SOD活力、蛋白表达水平逐渐下降,并呈剂量-效应关系。与高锰组比较,MT干预组自主运动和站立次数增加明显(P<0.05,P<0.01);γ-GCS、GSH-Px和SOD活力、阳性表达及蛋白水平均显著升高。结论本实验结果提示过量锰暴露可导致运动障碍及纹状体氧化损伤,褪黑素可能通过激活抗氧化酶GSH-Px、SOD和γ-GCS发挥对它的拮抗作用。
Objective To investigate the effects of melatonin on dyskinesia and striatum damage induced by manganese in mice. Methods Totally 84 mice were randomly divided into 6 groups: control group, low, middle and high Mn group, MT group and MT + high Mn group. Groups 5 and 6 were injected with 5 mg / kg MT subcutaneously in advance. After 2 hours, groups 2 to 4 and 6 were intraperitoneally injected with 12.5, 25, 50 and 50 mg / kg MnCl2, respectively, for 2 weeks. The autonomic activity of mice was observed and the vitality, expression and protein level of GSH-Px, SOD and γ-GCS were detected. Results With the increase of manganese concentration, the number of autonomic activity and standing gradually decreased. The activity and protein expression of γ-GCS, GSH-Px and SOD in the striatum decreased gradually and showed a dose-effect relationship. Compared with the high manganese group, the number of motoneuric movements and the number of standing increased significantly in the MT-treated group (P <0.05, P <0.01). The activity, positive expression and protein level of γ-GCS, GSH-Px and SOD were significantly increased. Conclusions Our results suggest that excess manganese exposure may lead to dyskinesia and striatal oxidative damage. Melatonin may exert its antagonistic effects by activating the antioxidant enzymes GSH-Px, SOD and γ-GCS.