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Food Chem Toxicol. 2011 Oct;49(10):2580-5. doi: 10.1016/j.fct.2011.06.076. Epub 2011 Jul 13.

Inhibitory effects of (-)-α-bisabolol on LPS-induced inflammatory response in RAW264.7 macrophages.

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1
Biospectrum Life Science Institute, Eines Platz 11th FL, 442-13 Sangdaewon Dong, Seoungnam City, 462-807 Gyunggi Do, Republic of Korea.

Abstract

Although (-)-α-bisabolol, a natural monocyclic sesquiterpene alcohol, is often used as a cosmetic soothing supplement, little is known about its mechanisms of anti-inflammatory effects. Therefore, this study was designed to investigate anti-inflammatory effects of (-)-α-bisabolol and its mechanisms of action. In this study, we found that (-)-α-bisabolol inhibited lipopolysaccharide (LPS)-induced production of nitric oxide (NO) and prostaglandin E(2) (PGE(2)) in RAW264.7 cells. In addition, expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) genes was reduced, as evidenced by Western blot and luciferase reporter assays for COX-2 and iNOS. To assess the mechanism of the anti-inflammatory property of (-)-α-bisabolol, its effects on the activity of AP-1 and NF-κB promoters were examined. LPS-induced activation of AP-1 and NF-κB promoters was significantly reduced by (-)-α-bisabolol. Consistently, (-)-α-bisabolol reduced LPS-induced phosphorylation of IκBα. In addition, while LPS-induced phosphorylation of ERK and p38 was attenuated by (-)-α-bisabolol, significant changes in the level of phosphorylated JNK were not observed. Our results indicate that (-)-α-bisabolol exerts anti-inflammatory effects by downregulating expression of iNOS and COX-2 genes through inhibition of NF-κB and AP-1 (ERK and p38) signaling.

PMID:
21771629
DOI:
10.1016/j.fct.2011.06.076
[Indexed for MEDLINE]

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