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目的研究PARK2基因在锰致大鼠运动功能降低中的作用。方法将30只SPF级SD雄性大鼠随机分成3组,每组10只。对照组:注射用生理盐水;低剂量组:Mn~(2+)1 mg/kg,换算成MnCl_2·4H2O为3.6 mg/kg;高剂量组:Mn~(2+)5 mg/kg,换算成MnCl_2·4H_2O为18 mg/kg。适应性喂养1周,通过腹腔注射染锰,1次/2 d,监测体重。通过体重变化的结果分析锰中毒对大鼠体重的影响;转棒实验检测大鼠运动协调能力;Y迷宫检测大鼠学习记忆能力;RT-PCR测定血液、纹状体、皮质内PARK2基因的表达,TH免疫组化染色观察染锰后雄性大鼠纹状体及黑质的病理改变。结果随着染锰剂量的增加大鼠体重增长明显减慢。对照组和高剂量组比较在转棒实验中总路程和总时间以及平均速度均有明显差异,对照组转动时间和路程明显长于染锰组,差异有统计学意义(P<0.05)。各组Y迷宫交替率差异无统计学意义。染锰组与对照组比较,全血、纹状体和皮质内PARK2的表达明显降低,差异有统计学意义(P<0.05)。光学显微镜下,TH免疫组化染色可见对照组黑质致密带的多巴胺能神经元数量较多,呈带状斜行排列,高剂量染锰组多巴胺能神经元几乎消失,残存神经元萎缩。结论锰对大鼠运动功能有一定影响,PARK2基因在对抗锰中毒大鼠模型的神经毒性中发挥了保护作用。
Objective To investigate the role of PARK2 gene in the reduction of motor function induced by manganese in rats. Methods Thirty SPF SD male rats were randomly divided into three groups of 10 rats. Control group: saline injection; low dose group: Mn 2+ (2+) 1 mg / kg, converted to MnCl 2 .4H 2 O 3.6 mg / kg; high dose group Mn 2+ 5 mg / kg Into MnCl 2 · 4H 2 O 18 mg / kg. Adaptive feeding for 1 week, by intraperitoneal injection of manganese, 1/2 d, weight monitoring. The body weight was analyzed by the results of body weight changes. The rats’ exercise capacity was evaluated by the rotation stick test. The learning and memory ability of rats was detected by Y maze. The expression of PARK2 gene in blood, striatum and cortex was detected by RT-PCR , TH immunohistochemical staining to observe the pathological changes of striatum and substantia nigra in the male rats after dyed with manganese. Results With the increase of manganese dose, rats’ weight gain slowed down significantly. The total distance and total time as well as the average speed in the control group and the high-dose group were significantly different in the rotary rod test. The rotation time and distance in the control group were significantly longer than those in the manganese-dosed group (P <0.05). There was no significant difference in the alternation rate of Y maze in each group. Compared with control group, the expression of PARK2 in whole blood, striatum and cortex decreased significantly in Mn-dyed group and control group (P <0.05). Under light microscope, TH immunohistochemical staining showed that there were many dopaminergic neurons in the substantia nigra compact zone in the control group, which were obliquely arranged in ribbons. The dopaminergic neurons in high-dose Mn-Zn group almost disappeared and the residual neurons atrophy. Conclusion Manganese has a certain effect on the motor function of rats, PARK2 gene plays a protective role in the neurotoxicity against rat model of manganese poisoning.