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目的探讨N-乙酰半胱氨酸(NAC)对PC12细胞的保护作用及其机制。方法采用神经毒素1μmol/L鱼藤酮处理PC12细胞24h,并在处理前30min加入500μmol/L的NAC进行干预,流式细胞术检测PC12细胞的凋亡率和活性氧水平,比色法检测还原型谷胱甘肽(GSH)水平。结果PC12细胞经1μmol/L鱼藤酮处理24h后,细胞凋亡率达41.9%,细胞内活性氧水平较对照组显著提高,而GSH水平显著下降(P<0.05);NAC干预后,能够明显抑制鱼藤酮的细胞毒性作用,与鱼藤酮组相比,细胞凋亡率和活性氧水平显著降低,GSH含量明显增加(P<0.05)。结论在帕金森病(PD)的细胞模型中,通过NAC的干预,能够明显保护PC12细胞,其保护机制与抗氧化能力有关。
Objective To investigate the protective effect of N-acetylcysteine (NAC) on PC12 cells and its mechanism. Methods PC12 cells were treated with neurotoxin 1 μmol / L rotenone for 24 h, and treated with 500 μmol / L NAC for 30 min before treatment. The apoptotic rate and reactive oxygen species of PC12 cells were detected by flow cytometry. Glutathione (GSH) levels. Results After treated with 1 μmol / L rotenone for 24 h, the apoptosis rate of PC12 cells reached 41.9%, the level of reactive oxygen species (ROS) in cells increased significantly and the level of GSH decreased significantly (P <0.05). After NAC intervention, Compared with rotenone group, the apoptotic rate and active oxygen level decreased significantly and the content of GSH increased significantly (P <0.05). Conclusion In the cell model of Parkinson’s disease (PD), PC12 cells can be significantly protected by the intervention of NAC, and its protective mechanism is related to the antioxidant capacity.