Epigallocatechin-3-gallate inhibits adipogenesis through down-regulation of PPARγ and FAS expression mediated by PI3K-AKT signaling in 3T3-L1 cells
Epigallocatechin-3-gallate inhibits adipogenesis through down-regulation of PPARγ and FAS expression mediated by PI3K-AKT signaling in 3T3-L1 cells
复制标题
表没食子儿茶素-3-没食子酸酯通过下调 3T3-L1 细胞中 PI3K-AKT 信号传导介导的 PPAR γ 和 FAS 表达来抑制脂肪生成
DOI：
10.1016/j.ejphar.2016.12.006
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发表时间：
2017-01-15
影响因子：
5
通讯作者：
Huang, Qiren
中科院分区：
文献类型：
--
作者：
Wu, Mengqing;Liu, Dan;Huang, Qiren
表没食子儿茶素没食子酸酯（Epigallocatechin-3-gallate，EGCG）是绿色茶的主要成分，具有抗炎、抗氧化、抗癌等多种生物活性。然而，其抗脂肪生成和潜在机制知之甚少。本研究的目的是探讨表没食子儿茶素没食子酸酯（EGCG）对3 T3-L1前脂肪细胞分化的影响及其可能的机制。3 T3-L1细胞在含有或不含指定浓度（10、50、100、200 μ M）的前脂肪形成混合物的条件下分别诱导分化2、4、6和8天。另外，在最佳EGCG浓度（100 μ M）下，用或不用SC 3036（PI 3 K激活剂，10 μ M）或SC 79（AKT激活剂，0.5 μ M）诱导另一批3 T3-L1细胞8天。MTT法检测细胞活力，油红O染色观察细胞形态。采用真实的时间定量PCR检测过氧化物酶体增殖物激活受体γ（PPARgamma）和脂肪酸合成酶（FAS）的mRNA水平，采用免疫印迹法检测PPARgamma FAS、磷脂酰肌醇3激酶（PI 3 K）、胰岛素受体底物1（IRS 1）、AKT和p-AKT的蛋白水平。结果表明，EGCG对3 T3-L1前脂肪细胞的成脂作用具有浓度依赖性。此外，抑制作用被SC 3036或SC 79逆转，表明EGCG的抑制作用是通过PI 3 K-AKT信号转导介导的，以下调PPAR γ和FAS表达水平。本研究结果揭示了EGCG抗脂肪形成作用及其潜在机制，并为中国绿色茶中的化合物提供了一种新的预防和治疗肥胖的潜力。
Epigallocatechin-3-gallate (EGCG), a major component in green tea, functions as extensive bioactivities including anti-inflammation, anti-oxidation, and anti-cancer. However, little is known about its anti-adipogenesis and underlying mechanisms. The purport of this study sought to investigate effects of EGCG on 3T3-L1 preadipocyte differentiation and to explore its possible mechanisms. The 3T3-L1 cells were induced to differentiate under the condition of pro-adipogenic cocktail with or without indicated EGCG concentrations (10, 50, 100, 200 mu M) for 2, 4, 6 and 8 days, respectively. Also, another batch of 3T3-L1 cells was induced under the optimal EGCG concentration (100 mu M) with or without SC3036 (PI3K activator, 10 mu M) or SC79 (AKT activator, 0.5 mu M) for 8 days. Subsequently, the cell viability was examined by MTT assay and the cell morphology was visualized by Oil red O staining. Finally, the mRNA levels including peroxisome proliferator activated receptor gamma (PPAR gamma) and fatty acid synthase (FAS) were detected by quantitative real time PCR, while the protein levels of PPAR gamma FAS, phosphatidylinositol 3 kinase (PI3K), insulin receptor substrate1(IRS1), AKT, and p-AKT were measured by immunoblotting analysis. Our results showed that EGCG inhibited adipogenesis of 3T3-L1 preadipocyte in a concentration-dependent manner. Moreover, the inhibitory effects were reversed by SC3036 or SC79, suggesting that the inhibitory effects of EGCG are mediated by PI3K-AKT signaling to down regulate PPAR gamma and FAS expression levels. The findings shed light on EGCG anti-adipogenic effects and its underlying mechanism and provide a novel preventive-therapeutic potential for obesity subjects as a compound from chinese green tea.