He Qiqiang, Huang Caixuan, Zhao Lihua, Feng Jing, Shi Qun, Wang Dengshun, Wang Suqing
Department of Nutrition and Food Hygiene, School of Public Health, Wuhan University Wuhan, Hubei 430071, China.
Int J Clin Exp Pathol. 2013;6(2):168-78. Epub 2013 Jan 15.
α-Naphthoflavone (α-NF) is a synthetic flavonone derivative and is well known as a potent inhibitor of aromatase in a variety of systems. However, its role in lipid metabolism remains far from understood. The aim of current study was to investigate the effects of α-NF on 3T3-L1 pre-adipocytes differentiation and the mechanism through which it acts. Treatment of 3T3-L1 cells with α-NF in conjunction with a hormone cocktail resulted in α-NF mediated suppression of adipocyte differentiation in a dose dependent manner. At the molecular level, our findings demonstrated that α-NF inhibited the mid and late phase, but not the early phase of adipogenic markers expression during 3T3-L1 adipogenesis. The phosphorylation of p38 was activated upon adipogenic stimulation, yet was substantially suppressed by α-NF treatment. α-NF also synergistically inhibited expression of the adipogenic marker peroxisome proliferator-activated receptor gamma (PPARγ) expression together with p38 selective inhibitor, SB203580. Our study demonstrated for the first time that α-NF is capable of suppressing 3T3-L1 adipocyte differentiation and that this effect likely occurs through repression of the p38MAPK signaling pathway.
α-萘黄酮（α-NF）是一种合成的黄酮酮衍生物，在多种系统中作为一种有效的芳香化酶抑制剂而广为人知。然而，其在脂质代谢中的作用仍远未被了解。本研究的目的是探讨α-NF对3T3-L1前脂肪细胞分化的影响及其作用机制。用α-NF联合激素鸡尾酒处理3T3-L1细胞，导致α-NF以剂量依赖的方式介导脂肪细胞分化的抑制。在分子水平上，我们的研究结果表明，α-NF抑制3T3-L1脂肪生成过程中脂肪生成标志物表达的中期和后期，但不抑制早期。p38的磷酸化在脂肪生成刺激时被激活，但α-NF处理可显著抑制。α-NF还与p38选择性抑制剂SB203580协同抑制脂肪生成标志物过氧化物酶体增殖物激活受体γ（PPARγ）的表达。我们的研究首次证明α-NF能够抑制3T3-L1脂肪细胞分化，并且这种作用可能通过抑制p38MAPK信号通路而发生。
