Curcumin inhibits adipogenesis induced by benzyl butyl phthalate in 3T3-L1 cells
Curcumin inhibits adipogenesis induced by benzyl butyl phthalate in 3T3-L1 cells
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DOI:
10.1016/j.taap.2017.05.036
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发表时间:
2017-08-15
影响因子:
3.8
通讯作者:
Fujimoto, Yohko
中科院分区:
文献类型:
--
作者:
Sakuma, Satoru;Sumida, Maki;Fujimoto, Yohko
Phthalates are a group of endocrine disrupting chemicals and may have contributed to the recent global obesity health crisis. Increased adipogenesis via the peroxisome proliferator-activated receptor gamma (PPAR gamma)-CCAAT-enhancer binding protein a (C/EBP alpha) pathway could be one critical mechanism responsible for phthalate-induced weight gain. On the other hand, curcumin has been shown to inhibit adipogenesis in cells and animal models. The present study was undertaken to evaluate, for the first time, whether curcumin could reduce adipogenesis induced by benzyl butyl phthalate (BBP) via downregulation of the PPAR gamma-C/EBP alpha pathway. 3T3-L1 preadipocytes were differentiated by treating them with insulin, dexamethasone, and 3-isobuty1-1-methylxanthine in the presence of BBP, with or without curcumin. Cells that were grown in the presence of BBP alone showed a significant increase in triacylglycerol (TG) levels. In addition, the number of Oil Red O-stained cells and the mRNA expression levels of PPAR gamma, C/EBP alpha, adiponectin, and tumor necrosis factor-alpha(TNF alpha) were significantly increased. However, treatment with BBP in combination with curcumin resulted in major reductions in TG levels, the numbers of Oil Red O-stained cells, and the mRNA expression levels of the four proteins. These results suggest that curcumin might be an inhibitor of BBP-induced weight gain and inflammation via stimulation of adipocyte differentiation and TNFa generation. Curcumin may, therefore, be a potential medication for preventing the harmful effects of phthalates. (C) 2017 Elsevier Inc All rights reserved.