首页> 外文期刊>Life sciences >(-)-Epigallocatechin-3-gallate blocks 3T3-L1 adipose conversion by inhibition of cell proliferation and suppression of adipose phenotype expression.
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(-)-Epigallocatechin-3-gallate blocks 3T3-L1 adipose conversion by inhibition of cell proliferation and suppression of adipose phenotype expression.

机译:(-)-Epigallocatechin-3-gallate通过抑制细胞增殖和抑制脂肪表型表达来阻止3T3-L1脂肪转化。

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AIMS: A major objective in the treatment of obese individuals is the development of agents that reduce body fat and improve metabolic homeostasis. Among a variety of biological effects, green tea exerts an anti-obesity effect; however, the mechanisms behind its activity on adipose tissue are uncertain. Tea contains high levels of (-)-epigallocatechin-3-gallate (EGCG), which is one of its main bioactive substances. Therefore, we studied the effects of EGCG on mouse embryonic fibroblast-adipose like cell line (3T3-L1) preadipocyte proliferation and differentiation. MAIN METHODS: 3T3-L1 cells were incubated with physiologically attainable (0.1-1 muM) and pharmacological (5muM, 10muM) concentrations of EGCG for various lengths of time. Cell proliferation was assessed by cell counting and cell cycle analysis. Adipose conversion was evaluated by lipid accumulation and expression of CCAAT/enhancer binding protein alpha (C/EBPalpha) and peroxisome proliferator-activated receptor gamma (PPARgamma) transcription factors. KEY FINDINGS: A dose dependent suppressive effect on preadipocyte proliferation was observed, with the highest reduction in cell number at 10muM EGCG. On the other hand, adipose conversion was fully inhibited with 10muM EGCG. Flow-cytometric analysis showed that 3T3-L1 cells treated with EGCG underwent an arrest of cell cycle at G2/M. The inhibition of the expression of C/EBPalpha and PPARgamma was accompanied by the inhibitory effect of EGCG. Microscopic observation showed that 3T3-L1 cells treated with EGCG maintained the fibroblastic shape and failed to accumulate cytoplasmic fat droplets even after the induction of differentiation. SIGNIFICANCE: Our results suggest that EGCG reduces adipogenesis through an arrest of cell cycle and a blockage of adipose phenotype expression. These results also suggest that the anti-obesity activity of green tea may be partially attributed to its suppressive effects in adipogenesis.
机译:目的:治疗肥胖个体的主要目的是开发减少体脂和改善代谢稳态的药物。在多种生物效应中,绿茶具有抗肥胖作用。然而,其在脂肪组织上的活性背后的机制尚不确定。茶含有高水平的(-)-epigallocatechin-3-gallate(EGCG),这是其主要的生物活性物质之一。因此,我们研究了EGCG对小鼠胚胎成纤维细胞脂肪样细胞系(3T3-L1)前脂肪细胞增殖和分化的影响。主要方法:将3T3-L1细胞与生理上可达到的浓度(0.1-1μM)和药理学浓度(5μM,10μM)的EGCG孵育不同的时间。通过细胞计数和细胞周期分析评估细胞增殖。通过脂质积累和CCAAT /增强子结合蛋白α(C / EBPalpha)和过氧化物酶体增殖物激活的受体γ(PPARgamma)转录因子的表达来评估脂肪转化。主要发现:观察到对前脂肪细胞增殖的剂量依赖性抑制作用,在10μMEGCG下细胞数量减少最多。另一方面,用10μMEGCG完全抑制了脂肪转化。流式细胞仪分析显示,用EGCG处理的3T3-L1细胞在G2 / M处停止了细胞周期。抑制C / EBPalpha和PPARgamma的表达伴随有EGCG的抑制作用。显微镜观察显示,EGCG处理的3T3-L1细胞即使在分化诱导后仍保持了成纤维细胞的形状,并没有积累细胞质脂肪滴。意义:我们的结果表明,EGCG通过阻止细胞周期和阻断脂肪表型表达来减少脂肪形成。这些结果还表明,绿茶的抗肥胖活性可能部分归因于其对脂肪形成的抑制作用。

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