Glucosamine inhibits LPS-induced COX-2 and iNOS expression in mouse macrophage cells (RAW 264.7) by inhibition of p38-MAP kinase and transcription factor NF-κB

✍ Scribed by Mohamed M. Rafi; Prem N. Yadav; Andrea O. Rossi

• Publisher: John Wiley and Sons
• Year: 2007
• Tongue: English
• Weight: 774 KB
• Volume: 51
• Category: Article
• ISSN: 1613-4125
• DOI: 10.1002/mnfr.200600226

✦ Synopsis

Abstract

Glucosamine supplements are very promising nonsteroidal anti‐inflammatory agents widely used for the treatment of arthritis in animals and humans. In this study, we have proposed the molecular mechanism underlying the anti‐inflammatory properties of glucosamine hydrochloride (GLN) using mouse macrophage cell line (RAW 264.7). Treatment with GLN inhibited LPS‐stimulated nitric oxide (NO) production. Western blotting and RT‐PCR analysis showed that GLN treatment decreased LPS‐induced inducible nitric‐oxide synthase (iNOS) and cyclooxygenase‐2 (COX‐2) protein and mRNA expression in RAW 264.7 cells, respectively. To further elucidate the mechanism of inhibitory effect of GLN, we studied the LPS‐induced phosphorylation of mitogen‐activated protein kinases (pp44/42 and pp38). Our results clearly indicated that GLN treatment resulted in a reduction of pp38, whereas activation of p44/42 was not affected. In addition, LPS‐induced activation of nuclear factor‐κB (NF‐κB) DNA binding suggests an inhibitory effect of GLN. These results indicate that GLN suppresses the LPS‐induced production of NO, expression of iNOS and COX‐2 by inhibiting NF‐κB activation and phosphorylation of p38 MAP kinase.