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microRNA-23b对Aβ25-35导致神经细胞凋亡的作用及机制研究

Effects and mechanisms of microRNA-23b on neuronal apoptosis induced by Aβ25-35

  • 摘要: 为了研究miR-23b对阿尔茨海默病(Alzheimer′s disease,AD)细胞模型的作用及机制,采用Aβ25-35诱导SH-SY5Y细胞损伤建立细胞模型;采用Annexin V-FITC/PI双染结合流式细胞术检测转染miR-23b对Aβ25-35诱导SH-SY5Y细胞凋亡情况的影响;采用JC-1探针检测转染miR-23b对Aβ25-35损伤SH-SY5Y细胞后细胞内线粒体膜电位的影响;采用Western blot检测转染miR-23b对Aβ25-35诱导SH-SY5Y细胞内凋亡相关蛋白Bax、Bcl-2以及自噬相关蛋白p62、LC3B、Beclin-1表达水平的变化。结果显示:miR-23b能够改善Aβ25-35诱导SH-SY5Y细胞的凋亡水平和异常的线粒体膜电位,并缓解Aβ25-35引起的神经细胞凋亡蛋白和自噬蛋白表达的异常,提示miR-23b能够改善Aβ25-35导致的凋亡通路和自噬通路异常,进而缓解Aβ25-35导致的神经细胞凋亡。

     

    Abstract: In this study, the effects and mechanisms of miR-23b in the AD cell model were explored. Aβ25-35 was used to induce neuronal injury model, and cell viabilities were detected by MTT assay. The effect of miR-23b on the apoptotic levels of Aβ25-35-induced SH-SY5Y cells was analyzed using Annexin V-FITC/PI detection kit. The effect of miR-23b on the mitochondrial membrane potential of Aβ25-35-induced SH-SY5Y cells was examined using JC-1 fluorescent probe. The levels of cell apoptosis-related proteins and autophagy-related proteins were detected by Western blot. The results showed that miR-23b could alleviate the apoptosis and the abnormal mitochondrial membrane potential in SH-SY5Y cells induced by Aβ25-35.This study suggested that miR-23b may attenuate Aβ25-35-induced neuronal apoptosis by regulating apoptosis and autophagy-related pathway.

     

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