Polygoni Rhizoma Inhibits Inflammatory Response through Inactivation of Nuclear Factor-kappaB and Mitogen Activated Protein Kinase Signaling Pathways in RAW264.7 Mouse Macrophage Cells

被引:16
|
作者
Seo, Hyuk-Jin [1 ]
Huh, Jeong-Eun [1 ]
Han, Jong-Hyun [1 ]
Jeong, Soo-Jin [1 ]
Jang, Jinsil [1 ]
Lee, Eun-Ok [1 ]
Lee, Hyo-Jung [1 ]
Lee, Hyo-Jeong [1 ]
Ahn, Kyoo Seok [1 ]
Kim, Sung-Hoon [1 ]
机构
[1] Kyung Hee Univ, Coll Oriental Med, Seoul 130701, South Korea
关键词
Polygoni Rhizoma; antiinflammation; nuclear factor-kappaB; mitogen-activated protein kinase; NITRIC-OXIDE SYNTHASE; B ACTIVATION; PROINFLAMMATORY CYTOKINES; GENE-EXPRESSION; CUSPIDATUM; P38; LIPOPOLYSACCHARIDE; CYCLOOXYGENASE; RISK; INOS;
D O I
10.1002/ptr.3530
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
The objective of this study was to determine the antiinflammatory effects of Polygoni Rhizoma (PR), an Oriental medicinal herb, in interleukin 1 beta (IL-1 beta) and lipopolysaccharide (LPS)-stimulated RAW264.7 mouse macrophage cells. PR significantly reduced the production of pro-inflammatory cytokines such as IL-6, tumor necrosis factor alpha (TNF-a) and pro-inflammatory mediators such as inducible nitric oxide synthase (iNOS), nitric oxide (NO), cyclooxygenase 2 (COX-2) and prostaglandin E2 (PGE2) even at a concentration of 1 mu g/mL in the cells. In addition, PR inhibited the transcriptional activity of NF-?B as well as the degradation and phosphorylation of inhibitory kappa B alpha (I?Ba). Furthermore, PR suppressed the phosphorylation of extracellular signal regulated kinase 1/2 (ERK1/2), p38 and c-Jun N-terminal kinase 1/2 (JNK1/2) in IL-1 beta and LPS-treated RAW264.7. The results suggest that PR exerts an antiinflammatory property by inhibiting iNOS, COX-2, TNF-a and IL-6 production in association with inactivation of the NF-?B and MAPK signaling pathways in RAW 264.7 cells. Copyright (C) 2011 John Wiley & Sons, Ltd.
引用
收藏
页码:239 / 245
页数:7
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