利福平抑制α-synuclein的聚集及对MPP^+诱导细胞损伤的拮抗作用  

Rifampicin inhibits the expression and aggregation of α-synuclein and antagonizes MPP^+-induced PC12 cells damage

作　　者：徐杰[1] 张国华[1] 陶恩祥[1] 

机构地区：[1]中山大学附属第二医院神经科,广东广州510120

出　　处：《中国病理生理杂志》2006年第10期2032-2035,共4页Chinese Journal of Pathophysiology

基　　金：广东省自然科学基金资助项目(No.04009355);广东省科技计划项目资助项目(No.2005B33801003)

摘　　要：目的:探讨利福平对帕金森病致病蛋白α-突触共核蛋白(α-synuc le in)聚集的影响,以及对1-甲基-4-苯基-吡啶离子(MPP+)诱导的细胞损伤的拮抗作用。方法:选用大鼠嗜铬细胞瘤株PC12细胞,利用MPP+诱导建立帕金森病细胞模型,利福平进行干预;采用MTT法检测细胞活性、W estern b lotting法检测α-synuc le-in表达及聚集,流式细胞仪检测细胞凋亡。结果:1 mmol/LMPP+组细胞活性明显低于对照组,细胞凋亡率和α-sy-nuc le in表达及聚集高于对照组;预先经过100、200和300μmol/L各浓度利福平处理后,MPP++利福平组细胞活性明显高于1 mmol/L MPP+组,而细胞凋亡率和α-synuclein表达及聚集均低于1 mmol/L MPP+组,并具有明显的剂量-效应关系。结论:利福平能够抑制α-synuclein的表达及聚集,并对MPP+诱导的PC12细胞损伤具有拮抗作用。AIM： To explore the effects of rifampicin on the expression and aggregation of α- synuelein and PC12 cell damage induced by MPP^＋ . METHODS： 1 - Methyl -4 - phenyl pyridinium （ MPP^＋ ） was added to make a model of parkinson＇s disease in rat pheochromoeytoma （PC12） cells. After co - incubation with rifampicin, cell viability was determined by MTT assay. The expression of α- synuclein was measured by Western blotting. Cell apoptosis was assessed by flow cytometry （FCM）. RESULTS ： Compared with control, the cell viability was significantly decreased. Cell apoptosis ratio, α-synuclein expression and aggregation were significantly increased in MPP^＋ group. Compared with MPP^＋ group, after co- incubation with rifampicin （100, 200 and 300 μmol/L） , cell viability was significantly increased, cell apoptosis rate and α-synuelein expression and aggregation were significantly decreased in a dose - dependent manner. CONCLUSION ： Rifampicin may be an inhibitor of the expression and aggregation α- synuclein and has a preteetive effect on PC12 cells treated with MPP^＋.

关 键 词：帕金森病 突触核蛋白 甲苯啶郿 利福平 

分 类 号：R363[医药卫生—病理学]