摘要
目的:探讨硫辛酸(LA)对脂多糖(LPS)诱导的帕金森病(PD)模型小鼠黑质多巴胺(DA)能神经元损伤的作用及机制。方法:10月龄雌性C57BL/6小鼠,随机分为生理盐水对照组、PD模型组和LA干预组。采用鼻腔滴入LPS制作PD小鼠模型,通过爬竿实验及酪氨酸羟化酶和p-NF-κB/p65的免疫组化技术观察LA对DA能神经元的保护作用。结果:LPS经鼻可以成功诱导小鼠PD模型,给予LA可明显恢复小鼠运动,减少黑质DA能神经元的丢失、抑制小胶质细胞及其NF-κB信号通路激活。结论:LA干预可缓解LPS经鼻诱导的小鼠PD行为学和病理学的改变,其作用机制可能与抑制脑内的炎症反应有关。
AIM: To evaluate the effect of lipoic acid( LA) on LPS-induced Parkinson disease( PD) model of mice. METHODS: Female C57 BL /6 mice of 10-month-old were randomly divided into saline control group,PD group and LA group. The PD mouse model was induced by intranasal instillation of LPS. Assays of tyrosine hydroxylase,microglia and nuclear factor kappa B( NF-κB) were performed by the methods of immunohistochemistry and Western blotting. RESULTS: Intranasal LPS instillation exhibited basic characteristics of PD model. However,LA administration significantly improved motor dysfunction,protected dopaminergic neurons from damage,and inhibited NF-κB activation in inflammatory microglia in the substantia nigra area of the brain. CONCLUSION: LA may exert a profound neuroprotective effect by anti-neuroinflammatory reaction to arrest the progression of PD.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2015年第2期201-206,共6页
Chinese Journal of Pathophysiology
基金
国家自然科学基金资助项目(No.81272163)
山西省青年自然科学基金资助项目(No.2012021034-2)
山西大同大学博士科研启动经费(No.2011-B-11)
山西大同大学研究所科研项目启动经费
山西中医学院"2011"培育计划项目(No.2011PY-1)
关键词
脂多糖
帕金森病
硫辛酸
小胶质细胞
Lipopolysaccharide
Parkinson disease
Lipoic acid
Microglia