Benzyl alcohol derivatives from the mushroom Hericium erinaceum attenuate LPS-stimulated inflammatory response through the regulation of NF-κB and AP-1 activity

• Published in: Immunopharmacology and immunotoxicology 2014-10, Vol.36 (5), p.349-354
• Main Authors: Noh, Hyung Jun, Yoon, Ju Young, Kim, Geum Sook, Lee, Seung Eun, Lee, Dae Young, Choi, Je Hun, Kim, Seung Yu, Kang, Ki Sung, Cho, Jae Youl, Kim, Ki Hyun
• Format: Article
• Language: English
• Subjects: Agaricales - chemistry; Animals; Anti-Inflammatory Agents - pharmacology; Benzyl Alcohol - isolation & purification; Benzyl Alcohol - pharmacology; Cell Line; Cell Survival - drug effects; Dinoprostone - biosynthesis; Erinacerin B; hericenone E; Hericium erinaceum; Inflammation - chemically induced; Inflammation - prevention & control; Lipopolysaccharides - antagonists & inhibitors; Mice; NF-kappa B - drug effects; nitric oxide; Nitric Oxide - biosynthesis; prostaglandin E; RAW 264.7 macrophage cells; Transcription Factor AP-1 - drug effects
• ISSN: 0892-3973; 1532-2513
• DOI: 10.3109/08923973.2014.947036

Abstract On the search for anti-inflammatory compounds from natural Korean medicinal sources, a bioassay-guided fractionation and chemical investigation of the MeOH extract from the fruiting bodies of Hericium erinaceum resulted in the isolation and identification of five benzyl alcohol derivatives (1-5). In this study, their anti-inflammatory effects on lipopolysaccharide (LPS)-induced production of pro-inflammatory mediators were examined using RAW 264.7 macrophage cells. The structures of isolates were identified by comparing their spectroscopic data with previously reported values. The analysis of their inhibitory activities on LPS-induced nitric oxide (NO) and prostaglandin E2 (PGE2) production in RAW 264.7 macrophage cells showed that erinacerin B (2) and hericenone E (4) decreased the levels of NO and PGE2 production in a concentration-dependent manner. Next, this study was performed to examine their mechanism of action on the regulation of NO and PGE2 production. Compounds 2 and 4 were found to block the LPS-induced phosphorylation of two major inflammatory transcription factors, NF-κB (p65/p50) and AP-1 (c-Jun and c-Fos). Taken together, these results suggest that down-regulation of LPS-induced NO and PGE2 production by compounds 2 and 4 is mediated through the modulation of NF-κB and AP-1 activation in macrophage cells. These results impact the development of potential health products for preventing and treating inflammatory diseases.