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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.
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页码:239 / 245
页数:7
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