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目的研究辛伐他汀对鱼藤酮诱导的三磷酸甘油醛脱氢酶(GAPDH)的聚集及对多巴胺能神经元凋亡的影响。方法体外培养PC12细胞,将细胞分为对照组、鱼藤酮处理组及鱼藤酮+辛伐他汀干预组;分别使用MTT试验了解药物干预对细胞活性的影响,使用生物化学方法检测细胞内丙二醛(MDA)含量、超氧化物歧化酶(SOD)活力以及谷胱甘肽(GSH)含量,使用免疫组化了解细胞内GAPDH定位以及聚集的变化,采用流式细胞仪检测细胞凋亡情况。结果鱼藤酮处理能够诱导细胞内氧化应激的产生并使得GAPDH表达增加并聚集。辛伐他汀的处理能够降低细胞内MDA含量,提高SOD和GSH活性并减少GAPDH蛋白的表达及聚集,流式细胞仪凋亡检测也发现辛伐他汀的处理能够减少鱼藤酮诱导的细胞凋亡。结论辛伐他汀可能通过抗氧化作用而减少鱼藤酮诱导的GAPDH的聚集及细胞凋亡。
Objective To investigate the effect of simvastatin on rotenone-induced accumulation of glyceraldehyde triphosphate dehydrogenase (GAPDH) and its effect on apoptosis of dopaminergic neurons. Methods PC12 cells were cultured in vitro. The cells were divided into control group, rotenone group and rotenone + simvastatin intervention group. MTT assay was used to investigate the effect of drug intervention on cell viability. The level of malondialdehyde (MDA) ), Superoxide dismutase (SOD) activity and glutathione (GSH) content were measured. Immunohistochemistry was used to investigate the location and aggregation of GAPDH in cells. Flow cytometry was used to detect apoptosis. Results Rotenone treatment induces intracellular oxidative stress and increases GAPDH expression and aggregation. Simvastatin treatment reduced MDA content in the cells, increased SOD and GSH activity, and decreased GAPDH protein expression and aggregation. Flow cytometry apoptosis assay also found that simvastatin treatment can reduce rotenone-induced apoptosis. Conclusion Simvastatin may reduce rotenone-induced GAPDH accumulation and apoptosis through antioxidation.