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

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。

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

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 immunocytochemical 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.