尼古丁对Parkinson小鼠黑质多巴胺能神经元及小胶质细胞的影响

EFFECTS OF NICOTINE ON THE DOPAMINERGIC NEURONS AND MICROGLIA IN THE SUBSTANTIA NIGRA OF PARKINSON’S DISEASE MICE

为探讨尼古丁对多巴胺能神经元的保护作用,本研究采用尼古丁(0.25mg/kg)预处理C57BL/6J小鼠,再给予1-甲基-2-乙基-1,2,3,6-四氢吡啶(MPTP;20mg/kg)诱导Parkinson病(PD)小鼠模型。通过行为学检测和中脑黑质致密部(SNc)的酪氨酸羟化酶(TH)以及OX-42的免疫组织化学染色,观察了尼古丁对PD小鼠的行为以及黑质多巴胺能神经元和小胶质细胞的影响。结果显示:经尼古丁预处理可以明显减轻PD小鼠的行为障碍,增加TH免疫阳性的多巴胺能神经元的数量,并且可以抑制SNc内小胶质细胞的增生。本研究结果提示,尼古丁可保护多巴胺能神经元,而抑制小胶质细胞的增生可能是其作用机制。

The present study was to investigate the protective effects of nicotine on dopaminergic neurons. C57BL/6J mice were injected with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine （MPTP, 20 mg/kg ） to establish Parkinson＇s disease （PD） model after pretreated with nicotine （0.25 mg/kg）. The effects of nicotine to PD mice were observed by behavioral test and immunecytechemical staining （ICC） for tyrosine hydroxylase （TH） and OX-42 in the compact part of the substantia nigra （SNc）. The results showed that nicotine markedly attenuated the dyskinesia of PD mice, increased the number of TH-positive dopaminergic neurons and simultaneously inhibited the activation of microglia in the SNc. These findings suggest that nicotine has protective effects on dopaminergic neurons in the MPTP-induced PD mice. It may be related to inhibiting the activation of microglia.