Abstract Title:

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

Abstract Source:

Food Chem Toxicol. 2011 Oct ;49(10):2580-5. Epub 2011 Jul 13. PMID: 21771629

Abstract Author(s):

Seungbeom Kim, Eunsun Jung, Jang-Hyun Kim, Young-Ho Park, Jongsung Lee, Deokhoon Park

Article Affiliation:

Seungbeom Kim


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.

Study Type : Human In Vitro

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