EGCG对H_2O_2诱导BV2细胞氧化损伤保护作用机制的研究  

The investigation on mechanism of(-)-Epigallocatechin-3-gallate(EGCG) against the BV2 cell damage induced by hydrogen peroxide(H_2O_2)

作　　者：范建东[1,2] 余巨明[1] 邵阳[3] 王莉[1] 张娟娟[2] 

机构地区：[1]川北医学院附属医院神经内科,四川南充637000 [2]川北医学院医学影像研究所,四川南充637000 [3]南京医科大学第二附属医院神经内科,江苏南京210000

出　　处：《中风与神经疾病杂志》2013年第6期516-519,共4页Journal of Apoplexy and Nervous Diseases

摘　　要：目的探讨EGCG对H2O2诱导BV2细胞氧化损伤的保护作用机制。方法以200μmol/L H2O2制备BV2细胞氧化应激损伤模型,用CCK-8法检测不同浓度EGCG(0、1、5、10、20、40、80μmol/L)的保护作用,Ho-echst33258染色法检测细胞的凋亡,Western bloting法检测caspase-9蛋白的表达。结果 10及20μmol/L的EGCG组保护效果较明显;EGCG保护组的凋亡细胞显著少于无保护组;20μmol/L EGCG保护组的caspase-9蛋白表达较无保护组明显下调(P=0.03<0.05)。结论 10及20μmol/L浓度的EGCG对H2O2诱导的BV2细胞损伤模型有保护作用,其机制可能是通过减少caspase-9蛋白的表达,进而部分阻断caspase-9所介导的caspases级联反应,减少BV2细胞的凋亡。Objective To investigate the protective mechanism of（-）-Epigallocatechin-3-gallate（EGCG） against the BV2 cell damage induced by hydrogen peroxide（H2O2）.Methods 200μmol/L H2O2 was used to make the oxidative stress injury mode of BV2 cells.The protective effect of different EGCG concentrations（0、1、5、10 、20、 40、 80μmol/L）,the apoptosis and the expression of caspase-9 were investigated by CCK-8 assay,immunofluorescence（Hoechst33258 staining）,and Western bloting,respectively.Results The concentrations of 10 and 20μmol/L EGCG produced distinctively protective effect on BV2 cells.The number of apoptotic BV2 cells in the two EGCG groups was significantly less than that in the non-EGCG treated group.In addition,the expression of caspase-9 was significantly downregulated in the 20μmol/L EGCG groups than that in the non-EGCG treated group（P=0.030.05）.Conclusion The concentions of 10 and 20μmol/L EGCG can effectively protect BV2 cell against the oxidative stress injury induced by H2O2.Its mechanism might result from its downregulation of caspase-9,which may block the caspase-9 mediated caspases cascade reaction to some extent,and therefore reduce the apoptosis of BV2 cells.

关 键 词：表没食子儿茶素没食子酸酯(EGCG) 凋亡 BV2细胞 

分 类 号：R742[医药卫生—神经病学与精神病学]