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目的探讨CDK5在鱼藤酮介导的SH-SY5Y细胞凋亡中的作用以及通过干预CDK5表达对细胞凋亡的影响。方法使用鱼藤酮处理多巴胺能神经元SH-SY5Y细胞,采用四甲基偶氮唑盐(MTT)法检测细胞活力,Annexin-V/PI染色,流式细胞仪检测不同实验组细胞凋亡率,采用Western blot法检测不同实验组CDK5的表达以及p25/p35蛋白的表达比。结果经鱼藤酮处理后细胞活力呈浓度依赖性下降,细胞凋亡率增高,且CDK5表达增高,p25/p35比值增高。CDK5抑制剂MDL28170或Olomoucine预处理细胞能够降低CDK5的表达水平,降低p25/p35蛋白的表达比,同时可以减轻鱼藤酮诱导的细胞损伤。结论 CDK5在鱼藤酮介导的SH-SY5Y细胞凋亡中可能发挥着重要作用,抑制CDK5的活性可能具有神经保护作用。
Objective To investigate the role of CDK5 in rotenone-induced apoptosis of SH-SY5Y cells and the effect of CDK5 on apoptosis. Methods Rotenone was used to treat SH-SY5Y cells. MTT assay was used to detect cell viability and Annexin-V / PI staining. Flow cytometry was used to detect apoptotic rates in different experimental groups. Western blot was used to detect the expression of CDK5 and p25 / p35 protein in different experimental groups. Results After rotenone treatment, the cell viability decreased in a concentration-dependent manner, and the apoptosis rate increased. The expression of CDK5 increased and the ratio of p25 / p35 increased. Pretreatment of cells with CDK5 inhibitor MDL28170 or Olomoucine decreased the expression of CDK5, decreased the expression of p25 / p35 protein, and reduced the rotenone-induced cell injury. Conclusion CDK5 may play an important role in rotenone-induced apoptosis of SH-SY5Y cells. Inhibition of CDK5 activity may have neuroprotective effects.