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作 者:邹少娜[1] 林敏[2] 伍石华[1] 王化修[1] 陈波[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》2011年第6期508-512,共5页Tumor
基 金:邵阳医学高等专科学校2010年度科研课题(编号:XK201001)
摘 要:目的:探讨表没食子儿茶素没食子酸酯(epigallocatechin-3-gallate,EGCG)对人胃癌BGC-823细胞增殖的影响及其可能的机制。方法:不同浓度EGCG单独或联合c-Jun氨基末端激酶(c-Jun N-terminal kinase,JNK)抑制剂SP600125作用BGC-823细胞后,应用MTT法检测BGC-823细胞的增殖抑制率,显微镜下观察细胞的形态学改变,FCM检测细胞凋亡率,蛋白质印迹法检测细胞中p-JNK和p-c-jun蛋白的表达情况,免疫细胞化学法检测细胞中caspase-3的表达。结果:EGCG可抑制BGC-823细胞的增殖(P<0.05),呈时间和剂量依赖效应;EGCG可诱导BGC-823细胞凋亡,细胞凋亡率呈剂量依赖效应(P<0.05);EGCG可上调BGC-823细胞中p-JNK、p-c-jun和caspase-3的表达(P<0.05)。EGCG引起的BGC-823细胞增殖抑制和caspase-3表达水平的上调可被SP600125部分抑制。结论:EGCG可诱导人胃癌BGC-823细胞凋亡,其作用机制可能与激活JNK信号转导途径并上调caspase-3的表达有关。Objective:To investigate the effect of epigallocatechin-3-gallate(EGCG) on the proliferation of human gastric cancer BGC-823 cells and to elucidate the possible mechanism.Methods:The proliferation inhibitory rates of BGC-823 cells treated with different concentrations of EGCG alone or in combination with c-Jun N-terminal kinase(JNK) inhibitor SP600125 were detected by MTT assay.The morphological changes of BGC-823 cells were observed under a microscope.The apoptosis rate of BGC-823 cells was determined by flow cytometry.The expression levels of p-JNK and p-c-jun proteins in BGC-823 cells were examined by Western blotting.The expression level of caspase-3 protein was detected by immunocytochemistry.Results:EGCG inhibited the proliferation of BGC-823 cells in dose-and time-dependent manners(P〈0.05).EGCG induced the apoptosis of BGC-823 cells in a dose-dependent manner(P〈0.05).The expression levels of p-JNK,p-c-jun and caspase-3 proteins in BGC-823 cells were up-regulated by EGCG(P〈0.05).The effects of EGCG on the proliferation inhibition and up-regulation of caspase-3 expression were partly inhibited by SP600125.Conclusion:EGCG can induce the apoptosis of BGC-823 cells.This effect may be associated with the activation of JNK transduction pathway and the up-regulation of caspase-3 expression.
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