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目的:探讨竹节参总皂苷对SH-SY5Y细胞的保护作用机制。方法:SH-SY5Y细胞随机分为正常对照组,H2O2模型组(600μmol/L H2O2),药物干预组(600μmol/L H2O2+0.1、1、5、20μg/m L竹节参总皂苷)。竹节参总皂苷预处理12 h后,再加入H2O2继续培养12 h。JC-1法检测线粒体膜电位变化,Western blotting检测Sirt1、PGC-1α、Foxo3a、LC3-Ⅱ和Beclin1的表达。结果:600μmol/L H2O2与SH-SY5Y共同孵育12 h后,线粒体膜电位下降,Sirt1、PGC-1α、Foxo3a、LC3-Ⅱ和Beclin1的蛋白表达下调,预孵育竹节参总皂苷能明显提高细胞线粒体的膜电位,增强Sirt1、PGC-1α、Foxo3a、LC3-Ⅱ和Beclin1的蛋白表达。结论:竹节参总皂苷对H2O2致SH-SY5Y神经细胞损伤具有保护作用,其机制可能与调节线粒体功能及自噬相关蛋白有关。
Objective: To investigate the protective effect of SSP on SH-SY5Y cells. Methods: SH-SY5Y cells were randomly divided into normal control group, H2O2 model group (600μmol / L H2O2), and drug intervention group (600μmol / L H2O2 + 0.1,1,5,20μg / m L total ginsenoside). Stems saponin pretreatment 12 h, then add H2O2 and cultured for 12 h. The changes of mitochondrial membrane potential were detected by JC-1 method. The expressions of Sirt1, PGC-1α, Foxo3a, LC3-Ⅱ and Beclin1 were detected by Western blotting. Results: After incubated with 600μmol / L H 2 O 2 and SH-SY5Y for 12 h, the mitochondrial membrane potential decreased and the protein expressions of Sirt1, PGC-1α, Foxo3a, LC3-Ⅱ and Beclin1 decreased. Mitochondrial membrane potential enhances the protein expression of Sirt1, PGC-1α, Foxo3a, LC3-Ⅱ and Beclin1. CONCLUSION: SSP can protect SH-SY5Y cells induced by H2O2. Its mechanism may be related to the regulation of mitochondrial function and autophagy-related proteins.