EGCG通过ERK1/2信号通路对BMMSCs成脂分化能力的影响

›› 2015, Vol. 35 ›› Issue (1): 24-28.

EGCG通过ERK1/2信号通路对BMMSCs成脂分化能力的影响

吴列红¹,朱慧勇²,刘建华³

1. 浙江省长兴县人民医院
2. 浙江大学医学院附属第一医院
3. 浙江大学附属第一医院

收稿日期:2014-04-14 修回日期:2014-06-25 出版日期:2015-01-28 发布日期:2015-01-28
通讯作者: 吴列红 E-mail:wuliehong2011@163.com

Inhibitory effect of EGCG on adipogenic differentiation of BMMSCs via ERK1/2 signaling pathway

Received:2014-04-14 Revised:2014-06-25 Online:2015-01-28 Published:2015-01-28
Contact: lie-hong wu E-mail:wuliehong2011@163.com

摘要/Abstract

摘要： 目的研究表没食子儿茶素没食子酸酯（EGCG）对骨髓间充质干细胞（BMMSCs）增殖及成脂分化的影响并探讨其中潜在的分子机制及信号通路。方法采用MTT分析EGCG对BMMSCs增殖的影响。通过油红O染色分析EGCG对细胞成脂分化能力的影响。应用实时荧光定量RT-PCR分析PPARγ、C/EBPα及C/EBPβ等基因的表达变化。同时，运用Western blot验证ERK1/2信号通路是否参与EGCG抑制BMMSCs成脂分化进程。结果低浓度EGCG（1~10 mmol/L）对BMMSCs细胞生长无明显作用，但高浓度EGCG（20~40 mmol/L）显著抑制细胞的增殖反应。通过抑制PPARγ、C/EBPα及C/EBPβ等关键转录因子的表达，EGCG明显抑制BMMSCs的成脂分化能力。ERK1/2通路在EGCG抑制BMMSCs成脂分化进程中扮演重要角色。结论 EGCG通过ERK1/2通路抑制BMMSCs的成脂分化能力。

关键词: 表没食子儿茶素没食子酸酯, 骨髓间充质干细胞, PPARγ, C/EBPα, C/EBPβ, ERK1/2

Abstract: Objective To determine the effect of epigallocatechin-3-gallate (EGCG) on the proliferation and adipogenic differentiation of bone marrow-derived mesenchymal stromal cells (BMMSCs) and to investigate the underlying molecular mechanism and involved signaling pathway. Methods 　To assess the effects of EGCG on the proliferation and adipogenic differentiation of BMMSCs,MTT and Oil red O staining were conducted respectively.The expression levels of key transcriptional factor during adipogenesis,including PPARγ,C/EBPα and C/EBPβ were measured by Real-time fluorescent quantitative RT-PCR.Also,Western blot was performed to confirm the role of ERK1/2 pathway in the inhibitory effects of EGCG on the adipogenic differentiation of BMMSCs. Results 　Although low concentrations of EGCG (1-10 mmol/L) exhibited no effects on BMMSCs growth,high levels of EGCG (20-40 mmol/L) significantly decreased the cell proliferative reaction.By inhibiting the expressions of PPARγ,C/EBPα and C/EBPβ,three key transcriptional factors in adipogenesis,EGCG also showed abilities to suppress the adipgenic differentiation of BMMSCs.ERK1/2 pathway was demonstrated to play an essential role in EGCG inhibiting adipogenesis. Conclusions 　EGCG can suppress the adipogenic differentiation of BMMSCs via ERK1/2 pathway.

Key words: Epigallocatechin-3-gallate, Bone marrow-derived mesenchymal stromal cells, PPARγ, C/EBPα, C/EBPβ, ERK1/2

中图分类号:

R329.29

吴列红朱慧勇刘建华. EGCG通过ERK1/2信号通路对BMMSCs成脂分化能力的影响[J]. 口腔医学, 2015, 35(1): 24-28.

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