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EGCG活化线粒体途径诱导人胃癌细胞凋亡 被引量：8

Induction of Apoptosis by Epigallocatechin-3-gallate via Activating Mitochondrial Signaling in Human Gastric Cancer Cells
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摘要 目的探讨表没食子儿茶素没食子酸酯(EGCG)通过活化线粒体途径诱导人胃癌BGC823细胞凋亡的作用机制。方法MTT法检测EGCG对BGC823细胞生长的影响;PI染色流式细胞术(FCM)分析测定细胞凋亡率;细胞线粒体跨膜电位(Δψm)用荧光染料罗丹明123染色FCM分析测定;Westernblot检测线粒体凋亡信号传导通路相关蛋白的表达。结果EGCG对BGC823细胞生长有显著抑制作用,呈时间和剂量依赖性。EGCG以剂量依赖方式诱导BGC823细胞凋亡。EGCG(20μg/mL、40μg/mL8、0μg/mL)作用48 h后,BGC823细胞中Δψm降低,细胞色素c(Cyt c)释放增加,caspase-9蛋白表达增加,呈剂量依赖性。结论EGCG通过活化线粒体信号传导途径诱导BGC823细胞凋亡。 Objective To elucidate the mechanism of apoptosis induced by epigallocatechin - 3 - gallate （EGCG） on human gastric cancer BGC823 cells via mitochondrial pathway. Methods The survival rate of BGC823 cells was detected by MTT assay. Cell apoptosis was determined by flow cytometry （FCM） using PI staining. Mitochondrial membrane potential was labeled by Rhodamine123 and examined by FCM. Western blot was used to analyze the expression of apoptosis mitochondrial signal transduction pathway related proteins. Results EGCG inhibited proliferation of BGC823 cells in a time - and dose - dependent manner. The apoptosis of BGC823 induced by EGCG was in a dose - dependent manner detected by FCM using PI staining. After treatment with 20 μg/mL,40μg/mL,80μg/mL of EGCG,Δψm was decreased, the releasing of cytochrome c was enhanced, the expression of caspase - 9 protein was increased in a dose - dependent manner. Conclusion EGCG induces apoptosis of BGC823 cells via activating mitochondrial signal tmnsduction pathway.
作者 刘晓萍 文小玲 邹少娜 王强 陈晓艳 罗招阳
机构地区 南华大学肿瘤研究所 南华大学医学院临床技能中心
出处 《南华大学学报（医学版）》 2007年第4期499-502,共4页 Journal of Nanhua University(Medical Edition)
关键词 EGCG 胃癌细胞 凋亡 线粒体跨膜电位 细胞色素C CASPASE EGCG gastric cancer cells apoptosis mitochondrial membrane potential cytochrome c caspase
分类号 R735.2 [医药卫生—肿瘤]
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参考文献10

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二级参考文献12

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共引文献13

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二级引证文献57

南华大学学报（医学版）
2007年 第4期

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