摘要
目的:观察利福平对鱼藤酮诱导帕金森病大鼠模型多巴胺神经元的保护作用以及对α-突触核蛋白形成和聚集的抑制作用。方法:持续3周给SD大鼠背部皮下注射鱼藤酮(1.5 mg·kg-1·d-1)以诱导其黑质多巴胺神经元丢失的同时,应用利福平(30 mg·kg-1·d-1)灌胃给药,并通过对大鼠进行行为学、黑质病理学、TH和α-突触核蛋白的免疫活性以及蛋白量的表达情况等方面的检测以证明利福平对帕金森病动物模型多巴胺神经元具有保护作用,对α-突触核蛋白的形成和聚集具有抑制作用。结果:低剂量长期背部皮下注射鱼藤酮可诱导SD大鼠出现行为学、黑质病理学、TH及α-突触核蛋白的免疫活性和蛋白量的表达情况的改变,而应用利福平灌胃后这些变化均显著减少。结论:利福平对鱼藤酮帕金森病大鼠模型的多巴胺神经元具有保护作用,此作用与其对模型中α-突触核蛋白的形成和聚集的抑制作用密切相关。
AIM ： To investigate the protective effect of rifampicin on rotenone - induced apoptosis of dopaminergic neurons and expression of α- synuclein in rats. METHODS ： Highly selective lesions and high expression of α- synuclein in nigrostriatal dopaminergic neurons in rats were induced by chronic subcutaneous exposure to rotenone at dose of 1.5 mg · kg^-1 · d^-1 for 3 weeks. At the same time, rifampicin was administered at dose of 30 mg · kg^-1 · d^-1 by intragastric administration for 3 weeks. The changes of behavior, pathology and immunoreactivity of TH and α- synuclein in SNc were observed. RESULTS ： Obvious changes of behavior, pathology and TH immunoreactivity in SNc were observed in male SD rats injected subcutaneously with rotenone and rifampicin protected rats against these toxic effects induced by rotenone. CONCLUSION： Rifampicin has extensive protective effects against rotenone - induced neurotoxicity, which is related to inhibiting the expression and aggregation of α- synuclein.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2008年第9期1751-1756,共6页
Chinese Journal of Pathophysiology
基金
广东省自然科学基金资助项目(No.04009355)
广东省科技计划资助项目(No.2005B33801003)
