中文摘要：

目的采用6-羟基多巴胺（6-OHDA）部分损伤大鼠帕金森病模型，探讨尼古丁保护多巴胺能神经元的机制。方法雌性SD大鼠60只采用随机数字表法分为三组：尼古丁高剂量治疗组（尼古丁2．0mg／kg腹膜腔内注射1、低剂量治疗组（尼古丁0．2mg／kg腹膜腔内注射1及模型对照组（生理盐水腹膜腔内注射1，每组20只。注射7d后，分别接受单侧纹状体内6-OHDA20μg注射，制作帕金森病模型。免疫组织化学及体视学方法定量分析黑质多巴胺能神经元和纹状体CD3、CD4和CD8阳性淋巴细胞数量。结果6-OHDA注射4周后，模型对照组注射侧黑质酪氨酸羟化酶（TH）免疫阳性细胞为对照侧的25．27％；而在尼古丁低剂量和高剂量组，注射侧的TH免疫阳性细胞分别为相应对照侧的64．97％和67．24％。各组各时间点6-OHDA注射侧纹状体有明显的T淋巴细胞浸润。尼古丁治疗组浸润的T淋巴细胞数较模型对照组明显减少，差异有统计学意义（P〈0．051，而CD4和CD8阳性细胞占总T淋巴细胞的比例在各组和各时间点基本一致。尼古丁治疗组和模型对照组比较差异无统计学意义（P〉0．051。结论尼古丁可抑制6-OHDA损伤诱导的T淋巴细胞浸润，对抗6-OHDA神经细胞毒性，保护多巴胺能神经元。

英文摘要：

Objective To explore the mechanism through which nicotine protects dopaminergic neurons against 6-hydroxydopamine （6-OHDA） toxicity in Parkinson＇s disease （PD） rat model. Methods Sixty Female SD rats were divided into 3 groups according to randomly digital table： High dosage group （nicotine 2 mg/kg, 5 injections i.p. per day at 2-h interval）, low dosage group （nicotine 0.2 mg/kg, 5 injections i.p. per day at 2-h interval） and model group （normal saline treatment）, n=20 each group. On day 8 after the treatment, a single injection of 20 μg of 6-OHDA was administered into striatum. Nicotine or normal saline was administered continuously daily until animals were killed. The dopaminergic neurons and CD3, CD4 and CD8-positive lymphocytes were analyzed quantitatively using immunohistochemistry and stereology. Results Four weeks after 6-OHDA administration, in the normal saline treated group, tyrosine hydroxylase-immunopositive cells in the substantia nigra of administered side was 25.27% of those in the one of non-administered side, and the immunopositive cells in 0.2 and 2 mg/kg nicotine treated groups were respectively 64.97% and 67.24% of those in the non-administered side. The loss of dopaminergic neurons induced by 6-OHDA in the substantia nigra was significantly less severe in the nicotine treatment groups （at both 0.2 and 2 mg/kg groups） than the saline treated group. T lymphocyte infiltration was markedly induced by 6-OHDA administration into striatum in all groups. In the striatum, we observed that the numbers ofCD3, CD4 and CD8-positive lymphocytes were reduced significantly in the nicotine treated animals as compared to saline controls （P〈0.05）. The proportions of CD4 and CD8 positive cells in the total T lymphocytes were roughly equivalent in all groups at all time points, and there were no significant difference between nicotine treated groups and saline treated group. Conclusion Nicotine may have a neuroprotective effect against 6-OHDA induced dooaminergic lesion by inhib