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目的探讨姜黄素(curcumin)对帕金森病(PD)多巴胺能神经元保护作用及其保护机制。方法 1-甲基-4-苯基吡啶离子(MPP)诱导人神经母细胞瘤细胞(SH-SY5Y)死亡作为PD体外研究模型,curcumin及SP600125(JNK抑制剂)处理,使用MTT法检测细胞生存率、Hoechst33258染色检测细胞形态变化、Western blot检测JNK通路蛋白含量变化。结果 MTT结果显示使用1μM姜黄素或5μMSP600125处理细胞2h,再给予3mMMPP处理细胞18h,与单独给予3mMMPP处理的细胞相比细胞活性显著增高;Hoechst33258染色结果显++示,MPP处理后,SH-SY5Y细胞的细胞核出现明显核固缩,使用姜黄素处理细胞可以减轻MPP对细胞的损伤;Western blot结果显示,经1μM姜黄素或5μMSP600125处理后,可明显抑制MPP诱导的JNK1、JNK2以及上游的MKK4和下游的c-Jun的活性。结论姜黄素保护MPP诱导的多巴胺能神经元损伤作用可能与抑制JNK信号转导通路相关。
Objective To investigate the protective effect of curcumin on dopaminergic neurons in Parkinson’s disease (PD) and its protective mechanism. Methods The death of human neuroblastoma cells (SH-SY5Y) induced by 1-methyl-4-phenylpyridinium ion (MPP) was used as a PD in vitro model. Curcumin and SP600125 (JNK inhibitor) Hoechst33258 staining was used to detect the morphological changes of cells. Western blot was used to detect the protein content of JNK pathway. Results MTT results showed that the cells treated with 1μM curcumin or 5μM SP600125 for 2h and then treated with 3mM MPP for 18h showed significantly higher cell viability than those treated with 3mM MPP alone. The results of Hoechst33258 staining showed that the expression of SH-SY5Y The results showed that MPP-induced JNK1, JNK2 and the upstream MKK4 and MPK-induced MKP induced by MPP were significantly inhibited by 1μM curcumin or 5μM SP600125 Downstream c-Jun activity. Conclusion Curcumin protects MPP-induced dopaminergic neurons injury may be related to inhibition of JNK signal transduction pathway.