利福平抑制α-synuclein的聚集及对MPP＋诱导细胞损伤的拮抗作用

目的： 探讨利福平对帕金森病致病蛋白α-突触共核蛋白（α-synuclein）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、Western blotting法检测α-synuclein表达及聚集，流式细胞仪检测细胞凋亡。 结果： 1 mmol/L MPP+组细胞活性明显低于对照组，细胞凋亡率和α-synuclein表达及聚集高于对照组；预先经过100、200和300 μmol/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。

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

AIM: To explore the effects of rifampicin on the expression and aggregation of α-synuclein 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 pheochromocytoma (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-synuclein 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 pretective effect on PC12 cells treated with MPP+.