Earticle

(-)-α-bisabolol is a sesquiterpene alcohol found in the oils of chamomile and other plants. (-)-α-bisabolol has been widely used in dermatological and cosmetic formulations as an anti-inflammatory agent. But so far there were no studies that show the inhibitory mechanism of (-)-α-bisabolol in inflammation-associated gene expression. Therefore, this study was designed to investigate the anti-inflammatory effect of (-)-α-bisabolol and its mechanisms of action. Among many pro-inflammatory mediators, we found that (-)-α-bisabolol inhibited LPS-induced production of nitric oxide (NO) and prostaglandin E2 (PGE2) in RAW264.7 cells. In addition, in iNOS and COX-2 promoter luciferase assays, (-)-α-bisabolol reduced LPS-induced activation of iNOS and COX-2 promoters. Protein levels of iNOS and COX-2 were also reduced by (-)-α-bisabolol in a concentration-dependent manner. These results suggest that (-)-α-bisabolol exerts anti-inflammatory effects by downregulating expression of iNOS and COX-2.In order to elucidate inhibitory mechanisms of (-)-α-bisabolol on expression of iNOS and COX-2, we investigated effects of (-)-α-bisabolol on LPS-induced activation of AP-1 and NF-kB elements which exist in the promoter of iNOS and COX-2 genes. LPS-induced activation of AP-1 and NF-kB promoters was significantly reduced by (-)-α-bisabolol, suggesting that AP-1 and NF-kB promoters are involved in (-)-α-bisabolol effects. To further confirm this, ELISA for phospho-IkBa and Western blot for phospho-p42/44mapk, phospho-p38mapk, and phospho-JNK were performed. (-)-α-bisabolol reduced LPS-induced phosphorylation of IkBa. In addition, while LPS-induced phosphorylation of p42/44mapk and p38mapk was attenuated by (-)-α-bisabolol, significant change in the level of phosphorylated JNK was not observed. Collectively, our results indicate that (-)-α-bisabolol exerts anti-inflammatory effects by downregulating expression of iNOS and COX-2 genes through the inhibition of NF-kB and AP-1 (p42/44mapk and p38mapk) signaling pathway and suggest that (-)-α-bisabolol may be introduced for the treatment of inflammatory diseases.

Edible bird's nest (EBN), made from the salivary excretions of the swiftlet, is one of the widely used health foods in asian communities. Until now, although EBN has been known to have immune-boosting and anti-viral activities, other functions have not been reported. This study is aimed to investigate the effects of EBN on proliferation of human adipose-derived stem cells (hADSCs) and its action mechanism. We found that EBN strongly promoted proliferation of hADSCs and nomal human fibroblasts (NHFs). Additionally, attempts to elucidate a possible mechanism underlying the EBN-mediated effects reveald that EBN induced production of IL-6 and VEGF, and that this was mediated through activation of NF-kB. Specially, WE found that production of IL-6 and VEGF was induced by EBN. In addition, EBN-induced production of IL-6 and VEGF was inhibited by PD98059, a p44/42 MAPK inhibitors, SB203580, a p38 MAPK inhibitor, and PDTC, a NF-kB inhibitor, but not SP600125, a JNK inhibitor. Similar to this, EBN-induced proliferation of hADSCs was also attenuated by PD98059, SB203580 and PDTC, but not SP600125. Taken together, these findings suggest that the EBN-induced proliferation of hADSCs primarily occurs through the increased expression of IL-6 and VEGF, which is mediated by the activation of NF-kB.