p38MAPK在EGCG诱导人胃癌MGC803细胞凋亡中的作用  

Role of p38 MAP kinase in epigallocatechin-3-gallate-induced apoptosis of human gastric cancer MGC803 cells

作　　者：邹少娜[1] 林敏[2] 王化修[1] 伍石华[1] 罗招阳[3] 

机构地区：[1]邵阳医学高等专科学校病理教研室,邵阳422000 [2]邵阳医学高等专科学校附属医院内科,邵阳422000 [3]南华大学肿瘤研究所,衡阳421001

出　　处：《肿瘤》2008年第9期763-766,共4页Tumor

摘　　要：目的:探讨p38丝裂原活化蛋白激酶(p38 mitogen-activaced protein kinase,p38MAPK)在表没食子儿茶素没食子酸酯(epigallocatechin-3-gallate,EGCG)诱导人胃癌MGC803细胞凋亡中的作用。方法:采用MTT法检测MGC803细胞的存活率,荧光显微镜观察和碘化丙啶染色FCM检测MGC803细胞凋亡率,Western印迹法检测MGC803细胞中p38MAPK蛋白及磷酸化p38MAPK蛋白的表达。结果:EGCG可诱导MGC803细胞凋亡,且p38MAPK被激活。用p38MAPK特异性抑制剂SB203580干预后,EGCG抑制MGC803细胞生长的作用明显减弱,细胞凋亡率下降,p38MAPK活性显著下降。结论:EGCG可诱导MGC803细胞凋亡,该作用可被SB203580显著抑制,提示EGCG可能通过激活p38MAPK使部分MGC803细胞凋亡。Objective： To determine the role of p38 mitogen-activated protein kinase（MAP） kinase signal transduction pathways in epigallocatechin-3-gallate （EGCG）-induced apoptosis in human gastric cancer MGC803 ceils. Methods： The viability of MGC803 cells was measured by MTr assay. Apoptosis of MGCS03 cells was observed by AO/EB fluorescence microscopy and detected by flow cytometry with PI staining. Expression of p38MAPK and phosphorylated p38 （pp38） MAPK were determined by Western blot analysis. Results： EGCG induced apoptosis of MGC803 cells and apparently increased the activity of pp38MAPK in MGC803 cells. However, after interference with pp38MAPK inhibitor, the inhibitory effect of EGCG on MGC803 cells was significantly weakened. The apoptotic rate of the cells and the activity of pp38MAPK also decreased dramatically. Conclusions ： EGCG can induce apoptosis of MGC803 cells. The effects could be markedly suppressed by pp38MAPK inhibitor, SB203580. EGCG induces apoptosis of MGC803 cells partly by activating p38 MAPK.

关 键 词：胃肿瘤 表没食子儿茶素没食子酸酯 丝裂原激活蛋白激酶激酶类 细胞凋亡 

分 类 号：R735.2[医药卫生—肿瘤]