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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

  • 1周薇,罗招阳,周秀田,宋颖,曹娟,陈科.表没食子儿茶素没食子酸酯诱导人胃癌MGC-803细胞凋亡及机制[J].中国肿瘤,2005,14(12):811-814. 被引量：14
  • 2Zhao Y, Yang LF, Ye M, et al. Induction of apoptosis by epigallocatechin - 3 - gallate via mitochondrial signal transduction pathway [J]. Preventive Medicine, 2004, 39:1172 - 1179.
  • 3Qanungo S, Das M, Haldar S. Epigallocatechin- 3 - gallate induces mitochondrial membrane depolarization and caspase - dependent apoptosis in pancreatic cancer cells [ J ]. Carcinogenesis, 2005, 26(5) :958 - 967.
  • 4Yang CS, Maliakal P, Meng X. Inhibition of carcinogenesis by tea[J]. Annu Rev Pharmacol Toxicol, 2002, 42: 25 - 54.
  • 5Khan N, Afaq F, Saleem M, et al. Targeting multiple signaling pathways by green tea polyphenol ( - ) - Epigallocatechin - 3 - gallate [J]. Cancer Res, 2006, 66(5):2500-2505.
  • 6Saeki K, Kobayashi N, Inazawa Y, et al. Oxidation- triggered c - Jun N - terminal kinase and p38 mitogen - activated protein kinase path- ways for apoptosis in human leukemic cells stimulated by EGCG: a distinct pathway from those of chemically induced and receptor- mediated apoptosis[J]. Siochem J, 2002, 368 (3): 705 - 720.
  • 7Roy AM, Balige MS, Katiyar SK. Epigallocatechin- 3 - gallate induces apoptosis in estrogen receptor-negative human breast carcinoma cells via modulation in protein expression of P53 and Bax and Caspase - 3 activation [J]. Mol Cancer Ther, 2005, 4(1): 81-90.
  • 8Lee YK, Brone ND, Strege AK, et al. VEGF receptor phosphorylation status and apoptosis is modulated by a green tea component, epigallocatechin- 3 - gallate, in B - cell chronic lymphocytic leukemia[J]. Blood, 2004, 104:788 - 794.
  • 9Qanungo S, Das M, Haldar S, et al. Epigallocatechin- 3 - gallate induces mitochondrial membrane depolarization and caspase-dependent apoptosis in pancreatic cancer cells [ J ]. Carcinogenesis, 2005, 26 (5) : 958 - 967.
  • 10Gupta S, Hastak K, Faq F, et al. Essential role of caspases in epigallocatechin - 3 - gal- late - mediated inhibtion of nuclear factor Kap- pa - B and inductin of apoptosis [ J ]. Oncogene, 2004, 21(1):26-29.

二级参考文献12

  • 1陈志鸿,罗招阳,周秀田,周薇,曹娟,陈科.EGCG诱导人胃癌细胞G1期阻滞[J].湖南师范大学学报（医学版）,2005,2(1):30-33. 被引量：9
  • 2Sachiko Okabe, Yumiko Ochiai, Miwa Aida, et al. Mechanistic Aspects of Green Tea as a Cancer Preventive: Effect of Components on Human Stomach Cancer Cell Lines [J]. Jpn J Cancer Res, 1999, 90:733-739.
  • 3Xiaohua Tan, Darong Hu, Shirong Li, et al. Differences of four catechins in cell cycle arrest and induction of apoptosis in LoVo cells [J].Cancer Letters, 2000, 158:1-6.
  • 4Adrian G, Paschka, Rachel, et al. Induction of apoptosis in prostate cancer cell lines by green tea component,epigallocatechine-3-gallate [J]. Cancer Letters, 1998, 130:1-7.
  • 5Hayakawa S, Saeki K, Sazuka M, et al. Apoptosis induction by epigallocatechin gallate involves its binding to Fas[J].Biochem Biophys Res Commun, 2001, 285 (5):1102-1106.
  • 6Yang E, Korsmeyer SJ. Molecular Than-atopsis: A Discourse on the BCL2 Family and Cell Death [J]. Blood,1996,88(2): 386-401.
  • 7Kuwana T, Mackey MR, Perkins G, et al. Bid, Bax, and lipids cooperate to form supramolecular openings in the outer mitochondrial membrane [J]. Cell, 2002, 111 (3) :331-342.
  • 8Martinou JC, Green DR. Breaking the mitochondrial barrier [J]. Nat Rev Mol Cell Biol, 2001, 2(1): 63-67.
  • 9Desagher S, Martinou JC. Mitochondria as the central control point of apoptosis [J]. Trends Cell Biol , 2000 ,10: 369-377.
  • 10Perez D, White E. TNF-α signals apoptosis through a Bid-dependent conformational change in Bax that is inhibited by E1B19K[J]. Mol Cell, 2000, 6:53-63.

共引文献13

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二级引证文献58

南华大学学报（医学版）
2007年 第4期

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