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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。
In order to explore the protective effects of nicotine on dopaminergic neurons, C57BL / 6J mice were pretreated with nicotine (0.25mg / kg) and then given 1-methyl-2-ethyl- Tetrahydropyridine (MPTP; 20 mg / kg) was induced in a Parkinson’s disease (PD) mouse model. The behavior of nicotine in PD mice and the effects of nigra dopaminergic neurons were observed through behavioral tests and tyrosine hydroxylase (TH) and OX-42 immunohistochemical staining of substantia nigra pars compacta (SNc) And microglia. The results showed that pretreatment with nicotine could significantly reduce the behavioral disturbance in PD mice, increase the number of TH-immunoreactive dopaminergic neurons, and inhibit the proliferation of microglia in SNc. The results suggest that nicotine can protect dopaminergic neurons, and inhibition of microglial proliferation may be its mechanism of action.