中文摘要：

目的：采用6-羟基多巴胺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：动物分别接受尼古丁（0．2mg／kg或2．0mg／kg）或生理盐水腹膜腔内注射。注射7天后，尼古丁高、低剂量治疗组和模型对照组动物分别接受纹状体内6-OHDA20μg注射，制作部分损伤帕金森病模型。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CD8^＋T淋巴细胞数量。结果：尼古丁低剂量治疗组和高剂量治疗组，6—0HDA注射侧的酪氨酸羟化酶免疫阳性细胞分别为相应对照侧的64．97±10．33％和67．24±12．67％；和模型对照组（25．27±11．79％）比较，差异有统计学意义（P〈0．01）。此外，尼古丁也可明显减少纹状体CD8^＋T淋巴细胞浸润（P〈0．05）。结论：尼古丁可能通过抑制CD8^＋T淋巴细胞浸润，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-OHDA toxicity in SD rat PD model. Methods： Rats received nicotine or saline treatment （two doses tested,0.2 mg/ kg and 2 mg/ kg, 5 injections i.p. per day at 2-h intervals）. 8 days after the treatment, a single injection of 20μg 6-OHDA was administered into striatum. Nicotine or saline was administered daily until animals were sacrificed. The dopaminergic neurons and CD8-positive lymphocytes were analyzed quantitatively using immunohistochemistry and stereology. Results： 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 in the saline treated group（P〈0.01）. In addition, the number of CD8-positive lymphocytes reduced significantly in the nicotine treated animals as compared to saline control（P〈0.05）. Conclusion： Our data suggest that nicotine may have a neuroprotective effect against 6-OHDA induced dopaminergic lesion by inhibiting the recruitment of CD8-positive lymphocytes.