p38MAPK 在EGCG 诱导人胃癌MGC803 细胞凋亡中的作用.doc

p38MAPK在EGCG诱导人胃癌MGC803细胞
凋亡中的作用
邹少娜1, 林敏2 ,王化修1, 伍石华1, 罗招阳3
邵阳医学高等专科学校病理教研室,湖南邵阳 422000;2. 邵阳医学高等专科学校附属医院内科,湖南邵阳 422000;3. 南华大学肿瘤研究所,湖南衡阳 421001)
摘要:目的探讨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。方法采用噻唑蓝比色法(MTT)检测MGC803细胞的存活率;采用荧光显微镜观察和PI染色流式细胞术,检测MGC803细胞凋亡率;采用Western blot方法检测MGC803细胞中磷酸化p38MAPK蛋白、p38MAPK蛋白的表达。结果 EGCG可诱导MGC803细胞凋亡,且p38MAPK激活。而SB203580(p38MAPK特异性抑制剂)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。
关键词: 胃肿瘤;表没食子儿茶素没食子酸酯; p38MAPK;细胞凋亡
中图分类号: 文献标识码: A
Role of p38 MAP Kinase in Epigallocatechin-3-gallate-Induced Apoptosis of Human Gastric Cancer MGC803 Cells
ZOU Shao-na1 , Lin Min2, WANG Hua-xiu1, WU Shi-hua1, LUO Zhao-yang3
(1 Department of Pathology, Shaoyang Medical College, Shaoyang, 422000, China; 2 Department of Medicine, Affiliated Hospital of Shaoyang Medical College, Shaoyang, 422000, China; 3. Instistute of Oncology, Nanhua University, Hengyang, 421001,China)
【基金项目】邵阳医学高等专科学校2008年校级课题
【作者简介】邹少娜(1981-),女,病理与病理生理学专业硕士,研究方向:肿瘤病因及其防治机制,
E-mail:hylzy2008@
Abstract【Objective】This study was designed to determine the role of p38 MAP kinase signal transduction pathways in epigallocatechin-3-gallate (EGCG)—induced apoptosis in human gastric cancer MGC803 cells. 【Methods】MGC803 cells growth inhibition was measured by MTT assay. Apoptosis of MGC803 cells was studied by AO/EB fluorescence stain and flow cytometry with PI staining. Expression of p38, phosphorylation of p38 (pp38) MAPK were determined by Western blot analysis. 【Results】EGCG could induce apoptosis of MGC803 cells and the activity of pp38MAPK in MGC803 cells was apparently increased. However, after treatment 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, and pp38MAPK inhibi