Bisphenol a diglycidyl ether (BADGE) suppresses tumor necrosis factor-α production as a PPARγ agonist in the murine macrophage-like cell line, raw 264.7

被引:37
|
作者
Nakamuta, M
Enjoji, M
Uchimura, K
Ohta, S
Sugimoto, R
Kotoh, K
Kato, M
Irie, T
Muta, T
Nawata, H
机构
[1] Kyushu Univ, Grad Sch Med Sci, Dept Med & Bioregulatory Sci, Higashi Ku, Fukuoka 8128582, Japan
[2] Kyushu Univ, Grad Sch Med Sci, Dept Mol & Cellular Biochem, Fukuoka, Japan
关键词
peroxisome proliferator-activated receptor gamma (PPAR gamma); bisphenol A diglycidyl ether (BADGE); lipopolysaccharide (LPS); tumor necrosis factor-alpha (TNF-alpha); nuclear factor-kappaB (NF-kappa B); coactivator;
D O I
10.1006/cbir.2001.0838
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Bisphenol A diglycidyl ether (BADGE) is a newly described peroxisome proliferator-activated receptor gamma (PPARgamma) antagonist in adipogenic cells. In contrast, in the macrophage-like cell line RAW 264.7, BADGE, like the PPARgamma agonist pioglitazone hydrochloride, not only increased promoter activity of the PPARgamma-luciferase reporter gene, but also suppressed lipopolysaccharide (LPS)-induced tumor necrosis factor-alpha (TNF-alpha) production. These results suggest that BADGE is a PPARgamma agonist in RAW 264.7 cells. Furthermore, overexpression of the coactivator p300 restored BADGE- or pioglitazone hydrochloride-suppressed promoter activity of the nuclear factor-kappa B (NF-kappaB)-luciferase reporter gene, suggesting that PPARgamma may interfere with NF-kappaB transcriptional activity via coactivator competition. (C) 2002 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:235 / 241
页数:7
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