Suppressive Effects of Quercetin-3-O-(6?-Feruloyl)-ss-D-Galactopyranoside on Adipogenesis in 3T3-L1 Preadipocytes Through Down-regulation of PPAR? and C/EBPa Expression
文献类型: 外文期刊
第一作者: Yang, Lei
作者: Yang, Lei;Zhang, Ya-Ou;Cai, Guo-Ping;Yang, Lei;Zhang, Ya-Ou;Cai, Guo-Ping;Li, Xiao-Fan;Gao, Lei
作者机构:
关键词: quercetin-3-O-(6?-feruloyl)-ss-D-galactopyranoside;quercetin;adipogenesis;PPAR;C;EBPa
期刊名称:PHYTOTHERAPY RESEARCH ( 影响因子:5.878; 五年影响因子:5.286 )
ISSN: 0951-418X
年卷期: 2012 年 26 卷 3 期
页码:
收录情况: SCI
摘要: Obesity is a chronic, costly disease, and flavonoids such as quercetin have been proven to play protective roles against it. This study investigated the suppressive effect of quercetin-3-O-(6?-feruloyl)-beta-D-galactopyranoside (QFG) on adipogenesis of 3T3-L1 preadipocytes. Quercetin-3-O-(6?-feruloyl)-beta-D-galactopyranoside and quercetin were both extracted from Psidium guajava (Myrtaceae, commonly known as guava) leaves and were evaluated for their suppressive effect on adipogenesis by means of oil red O staining and triglyceride assay. It was shown that QFG inhibited adipogenesis in a dose- and time-dependent manner, and it exerted a stronger effect than did quercetin at the same concentration. Quantitative real-time polymerase chain reaction and western blotting were conducted to further examine the differentiation expression of marker genes and transcriptional factors. Both mRNA and protein expression of the key adipogenic transcriptional factors, peroxisome proliferator-activated receptor gamma (PPAR?) and CCAAT (cytidine-cytidine-adenosine-adenosine-thymidine)/enhancer-binding protein alpha (C/EBPa), were inhibited by QFG. Moreover, the mRNA expression patterns of key participants in the Wnt beta-catenin pathway were not altered during the QFG-induced adipogenesis inhibition. These results suggest that QFG effectively suppresses adipogenesis and that it exerts its role mainly through the significant down-regulation of PPAR? and C/EBPa and, probably, via a Wnt beta-catenin independent pathway. Copyright (c) 2011 John Wiley & Sons, Ltd.
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