| 蒋莎莉1,2 罗招阳2 曹慧秋1 胡玉林1 吴海燕1.EGCG 对人结肠癌HT-29 细胞凋亡的影响以及对MMP-2，RECK 的
调节作用[J].,2011,11(12):2258-2262 |
| EGCG 对人结肠癌HT-29 细胞凋亡的影响以及对MMP-2，RECK 的
调节作用 |
| Effects of Epigallaocatechin-3-gallate on Apoptosis of Human Colon CancerHT-29 Cell and MMP-2,RECK |
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| DOI： |
| 中文关键词: 结肠癌 表没食子儿茶素没食子酸酯 凋亡 |
| 英文关键词: Colon cancer EGCG Apoptosis |
| 基金项目:湖南省郴州市第一人民医院科研资助项目（2010-048） |
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| 中文摘要: |
| 目的：观察表没食子儿茶素没食子酸酯（Epigallaocatechin-3-gallate, EGCG）对人结肠癌HT-29 细胞增殖和凋亡的影响，并探
讨其对MMP-2，RECK 的调节作用。方法：体外培养人结肠癌HT-29 细胞，MTT 比色法检测EGCG 对HT-29 细胞的生长抑制作
用；Histone/DNA ELISA 检测细胞凋亡；FITC 标记Annexin-V/PI 双染流式细胞术分析凋亡细胞百分率；Western Blot 和RT-PCR
方法检测EGCG 对MMP-2，RECK 蛋白和mRNA 表达的影响。结果：EGCG 呈浓度和时间依赖性抑制HT-29 细胞的增殖，并且
增加HT-29 细胞Histone/DNA 碎片的渗漏；EGCG 诱导HT-29 细胞凋亡百分率增高；EGCG 抑制MMP-2 蛋白和mRNA 的表达，
促进RECK 蛋白和mRNA 的表达。结论：EGCG 抑制人结肠癌HT-29 细胞的增殖，促进其凋亡，并且呈浓度和时间依赖性；其作
用机制可能与其下调MMP-2 蛋白和mRNA 的表达、上调RECK 蛋白和mRNA 的表达有关。 |
| 英文摘要: |
| Objective: To investigate the effects of green tea extract epigallocatechin-3-gallate (EGCG) on proliferation and
apoptosis of human colon cancer cell line HT-29, explore it's regulation of MMP-2, RECK. Methods: HT-29 cells were cultured in vitro.
MTT assay was used to test the inhibitory effects of EGCG on proliferation in HT-29 cells. Histone/DNA fragments in medium were
determined using ELISA assay. Flow cytometry with FITC labeled annexin V staining was used to determine the percentage of apoptotic
cells. Western Blotting was used to analyze the expression of MMP-2 and RECK. And the mRNA expression was detected by RT-PCR.
Results: MTT assay has shown that EGCG inhibited HT-29 cells and exhibited a dose-time-dependent modal, and increased leakage of
the histone/DNA fragments in HT-29 cells. EGCG significantly induced increase of the percentage of apoptotic cells, down-regulated the
expression of MMP-2 protein and mRNA levels, and up-regulated the expression of RECK protein and mRNA levels. Conclusion: EGCG
inhibits proliferation and promotes apoptosis of HT-29 cells in a concentration dependent manner, and the mechanism is associated with
downregulation of MMP-2 and upregulation of RECK in protein and mRNA levels. |
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