ScholarWorks@숙명여자대학교

초록

In this study, the antiobesity effects of baicalin, 5,6-dihydroxyflavone-7-glucuronic acid, were characterized using an in vitro system of adipogenesis, i.e. fat cell formation. Baicalin-treatment of 3T3-L1 preadipocytes was shown to inhibit triglyceride accumulation and lipid droplet formation during induced adipogenesis. Microarray analyses showed that baicalin modulated the expression of genes located in pathways such as adipogenesis, cholesterol biosynthesis, focal adhesion and others. In the adipogenesis pathway, treatment with baicalin significantly down-regulated terminal differentiation markers of adipocytes including fatty acid binding protein 4. The effects of baicalin on the core part of the adipogenesis pathway, however, were paradoxical; the expression levels of CCAAT/enhancer binding protein (C/EBP)beta and C/EBP delta were up-regulated, while the expression levels of the peroxisome proliferator-activated receptor (PPAR)gamma and C/EBP alpha were down-regulated. The antiadipogenic mechanisms of baicalin can be explained by its effects on the upstream part of adipogenesis pathway; baicalin not only up-regulates the antiadipogenic regulators, C/EBP gamma, C/EBP homologous protein and Kruppel-like factor (KLF)2, but also down-regulates the proadipogenic regulator, KLF15. The overall effects of baicalin on these upstream regulators of adipogenesis were antiadipogenic, resulting in the down-regulation of downstream genes and the inhibition of cellular fat accumulation. Copyright (C) 2009 John Wiley & Sons, Ltd.

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