N-乙酰半胱氨酸对PC12细胞的保护作用研究

Protective effect of N-acetylcysteine against rotenone-induced apoptosis in PC12 cells

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 in rotenone-induced cell injury. Methods PC12 cells were treated with 1μmol/L of rotenone for 24 h. Additionally,N- acetylcysteine（500 μmol/L） was added 30rain before rotenone treatment. Apoptosis and reactive oxygen species （ROS） were both determined with flow cytometry（FCM）. Glutathione assay kit was used to assess the level of intracellular glutathione. Results After rotenone treatment,the apoptosis rate of PC12 cells was up to 41.9%. Rotenone treatment also enhanced the production of ROS and decreased the level of GSH（P〈0. 05）. Pretreatment with NAC partially inhibited the toxic effect of rotenone, suggested by decreased apoptosis rate and ROS formation and elevated GSH levels when comparing with rotenone group. Conclusions In this cell model of Parkinson＇s disease, NAC protected PC12 cells against the toxicity of rotenone and the mechanism was associated with its antioxidant ability.