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

Although (-)-alpha-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 (-)-alpha-bisabolol and its mechanisms of action. In this study, we found that (-)-alpha-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 (-)-alpha-bisabolol, its effects on the activity of AP-1 and NF-kappa B promoters were examined. LPS-induced activation of AP-1 and NF-kappa B promoters was significantly reduced by (-)-alpha-bisabolol. Consistently, (-)-alpha-bisabolol reduced LPS-induced phosphorylation of I kappa B alpha. In addition, while LPS-induced phosphorylation of ERK and p38 was attenuated by (-)-alpha-bisabolol, significant changes in the level of phosphorylated JNK were not observed. Our results indicate that (-)-alpha-bisabolol exerts anti-inflammatory effects by downregulating expression of iNOS and COX-2 genes through inhibition of NF-kappa B and AP-1 (ERK and p38) signaling. (C) 2011 Published by Elsevier Ltd.