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

被引:35
作者
Rafi, Mohamed M. [1 ]
Yadav, Prem N. [1 ]
Rossi, Andrea O. [1 ]
机构
[1] Rutgers State Univ, Cook Coll, Dept Food Sci, New Brunswick, NJ 08901 USA
关键词
COX-2; glucosamine; iNOS; NF-kappa B; p38; MAPK;
D O I
10.1002/mnfr.200600226
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
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-kappa B (NF-KB) 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-KB activation and phosphorylation of p38 MAP kinase.
引用
收藏
页码:587 / 593
页数:7
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