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J. Lipid Res.
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A more recent version of this article appeared on January 1, 2010

Papers In Press, published online ahead of print July 3, 2009
J. Lipid Res., doi:10.1194/jlr.M900255-JLR200
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Submitted on May 26, 2009
Revised on June 29, 2009
Accepted on July 3, 2009

Carvacrol, a component of thyme oil, activates PPARalpha and gamma , and suppresses COX-2 expression

Mariko Hotta, Rieko Nakata, Michiko Katsukawa, Kazuyuki Hori, Saori Takahashi, and Hiroyasu Inoue

Food Science & Nutrition, Nara Women's University, Nara, Nara 630-8506

Corresponding Author: inoue{at}cc.nara-wu.ac.jp

Cyclooxygenase-2 (COX-2), the rate-limiting enzyme in prostaglandin biosynthesis, plays a key role in inflammation and circulatory homeostasis. Peroxisome proliferator-activated receptors (PPARs) are ligand-dependent transcription factors belonging to the nuclear receptor superfamily and are involved in the control of COX-2 expression, and vice versa. Here, we show that COX-2 promoter activity was suppressed by essential oils derived from thyme, clove, rose, eucalyptus, fennel, and bergamot in cell-based transfection assays using bovine arterial endothelial cells. Moreover, from thyme oil, we identified carvacrol as a major component of the suppressor of COX-2 expression and an activator of PPARa and g. PPARg-dependent suppression of COX-2 promoter activity was observed in response to carvacrol treatment. In human macrophage-like U937 cells, carvacrol suppressed lipopolysaccharide-induced COX-2 mRNA and protein expression, suggesting that carvacrol regulates COX-2 expression through its agonistic effect on PPARg. These results may be important in understanding the anti-inflammatory and anti-lifestyle-related disease properties of carvacrol.


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