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绿茶多酚表没食子儿没食子酸酯抑制3T3-L1脂肪细胞的脂肪生成并诱导其凋亡。

Green tea polyphenol epigallocatechin gallate inhibits adipogenesis and induces apoptosis in 3T3-L1 adipocytes.

作者信息

Lin Ji, Della-Fera Mary Anne, Baile Clifton A

机构信息

444 Edgar L. Rhodes Center for Animal and Dairy Science, University of Georgia, Athens, GA 30602-2771, USA.

出版信息

Obes Res. 2005 Jun;13(6):982-90. doi: 10.1038/oby.2005.115.

Abstract

OBJECTIVE

Green tea catechins have been shown to promote loss of body fat and to inhibit growth of many cancer cell types by inducing apoptosis. The objective of this study was to determine whether epigallocatechin gallate (EGCG), the primary green tea catechin, could act directly on adipocytes to inhibit adipogenesis and induce apoptosis.

RESEARCH METHODS AND PROCEDURES

Mouse 3T3-L1 preadipocytes and mature adipocytes were used. To test the effect of EGCG on viability, cells were incubated for 3, 6, 12, or 24 hours with 0, 50, 100, or 200 microM EGCG. Viability was quantitated by MTS assay. To determine the effect of EGCG on apoptosis, adipocytes were incubated for 24 hours with 0 to 200 microM EGCG, then stained with annexin V and propidium iodide and analyzed by laser scanning cytometry. Both preadipocytes and adipocytes were also analyzed for apoptosis by terminal deoxynucleotidyl transferase dUTP nick-end labeling assay. To determine the effect of EGCG on adipogenesis, maturing preadipocytes were incubated during the 6-day induction period with 0 to 200 microM EGCG, then stained with Oil-Red-O and analyzed for lipid content.

RESULTS

EGCG had no effect on either viability or apoptosis of preconfluent preadipocytes. EGCG also did not affect viability of mature adipocytes; however, EGCG increased apoptosis in mature adipocytes, as demonstrated by both laser scanning cytometry and terminal deoxynucleotidyl transferase dUTP nick-end labeling assays. Furthermore, EGCG dose-dependently inhibited lipid accumulation in maturing preadipocytes.

DISCUSSION

These results demonstrate that EGCG can act directly to inhibit differentiation of preadipocytes and to induce apoptosis of mature adipocytes and, thus, could be an important adjunct in the treatment of obesity.

摘要

目的

绿茶儿茶素已被证明可促进体内脂肪减少,并通过诱导细胞凋亡抑制多种癌细胞类型的生长。本研究的目的是确定表没食子儿茶素没食子酸酯(EGCG),即主要的绿茶儿茶素,是否能直接作用于脂肪细胞以抑制脂肪生成并诱导细胞凋亡。

研究方法与步骤

使用小鼠3T3-L1前脂肪细胞和成熟脂肪细胞。为测试EGCG对细胞活力的影响,将细胞与0、50、100或200微摩尔/升的EGCG孵育3、6、12或24小时。通过MTS法测定细胞活力。为确定EGCG对细胞凋亡的影响,将脂肪细胞与0至200微摩尔/升的EGCG孵育24小时,然后用膜联蛋白V和碘化丙啶染色,并通过激光扫描细胞术进行分析。前脂肪细胞和脂肪细胞也通过末端脱氧核苷酸转移酶dUTP缺口末端标记法进行凋亡分析。为确定EGCG对脂肪生成的影响,在6天的诱导期内,将正在成熟的前脂肪细胞与0至200微摩尔/升的EGCG孵育,然后用油红O染色并分析脂质含量。

结果

EGCG对未汇合的前脂肪细胞的活力或凋亡均无影响。EGCG也不影响成熟脂肪细胞的活力;然而,激光扫描细胞术和末端脱氧核苷酸转移酶dUTP缺口末端标记法均表明,EGCG可增加成熟脂肪细胞的凋亡。此外,EGCG剂量依赖性地抑制正在成熟的前脂肪细胞中的脂质积累。

讨论

这些结果表明,EGCG可直接作用于抑制前脂肪细胞的分化,并诱导成熟脂肪细胞的凋亡,因此可能是治疗肥胖症的重要辅助药物。

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