表没食子儿茶素促进Nrf2的核转位减轻Aβ25-35对SH-SY5Y细胞的损伤

Epigallocatechin promotes nuclear translocation of Nrf2 to reduce damage of Aβ25-35 in SH-SY5Y cells

目的研究表没食子儿茶素(epigallocatechin,EGC)对Aβ25-35损伤SH-SY5Y细胞的保护作用及机制。方法采用Aβ25-35损伤SH-SY5Y细胞,MTT和LDH法,考察EGC对SH-SY5Y细胞活力的影响。应用DCFH-DA荧光探针检测细胞内ROS水平,通过测定细胞内SOD、GSH-Px和MDA活性,考察细胞氧化应激水平。Westernblot测定细胞中Nrf2、NQO1、HO-1、Prdx6和Trx1蛋白含量。结果Aβ25-35损伤SH-SY5Y细胞,导致细胞存活率明显降低。5、10、20μmol·L^-1EGC能够减轻Aβ25-35诱导的SH-SY5Y细胞损伤及LDH释放。而且EGC能够减少Aβ25-35诱导的细胞内ROS水平的增加,减轻氧化应激损伤。同时,EGC能够明显增强Aβ25-35损伤后Nrf2、NQO1、HO-1、Prdx6和Trx1的表达。结论EGC能够抑制Aβ25-35诱导的SH-SY5Y细胞损伤,通过促进Nrf2核转位,提高抗氧化水平,降低Aβ25-35神经毒性。

Aim To investigate the protective effect of epigallocatechin(EGC) on SH-SY5Y cells induced by Aβ25-35 injury.Methods MTT and LDH assay were employed to investigate the effects of EGC on viability of SH-SY5Y cells.DCFH-DA fluorescent probe was used to detect the intracellular ROS levels,and the activity of SOD,GSH-Px and MDA in cells was measured to investigate the level of oxidative stress in cells.Western blot analysis was used to determine Nrf2,NQO1,HO-1,Prdx6 and Trx1 levels in cells.Results SH-SY5Y cells were injured by Aβ25-35 treatment,and the cell viability was significantly reduced.5,10 and 20 μmol·L -1 of EGC alleviated Aβ25-35 induced SH-SY5Y cell injury and reduced LDH release.In addition,EGC could reduce the intracellular ROS level induced by Aβ25-35 and inhibit oxidative stress.At the same time,EGC could significantly enhance the expression of Nrf2,NQO1,HO-1,Prdx6 and Trx1 after Aβ25-35 injury.Conclusions EGC could inhibit Aβ25-35-induced SH-SY5Y cell injury,increase the cells antioxidant levels and reduce the neurotoxicity of Aβ25-35 by promoting nuclear translocation of Nrf2.