Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 11, Issue 8, Pages 1095-1102Publisher
ELSEVIER
DOI: 10.1016/j.intimp.2011.03.005
Keywords
Arctigenin; Anti-inflammation; JAK-STAT; iNOS
Categories
Funding
- National Nature Science Foundation of China [81072433, 31071000, 30770842, 30771979]
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
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Arctigenin has been demonstrated to have an anti-inflammatory function, but the precise mechanisms of its action remain to be fully defined. In the present study, we determined the effects of arctigenin on lipopolysaccharide (LPS)-induced production of proinflammatory mediators and the underlying mechanisms involved in RAW264.7 cells. Our results indicated that arctigenin exerted its anti-inflammatory effect by inhibiting ROS-dependent STAT signaling through its antioxidant activity. Arctigenin also significantly reduced the phosphorylation of STAT1 and STAT 3 as well as JAK2 in LPS-stimulated RAW264.7 cells. The inhibitions of STAT1 and STAT 3 by arctigenin prevented their translocation to the nucleus and consequently inhibited expression of iNOS, thereby suppressing the expression of inflammation-associated genes, such as IL-1 beta, IL-6 and MCP-1, whose promoters contain STAT-binding elements. However, COX-2 expression was slightly inhibited at higher drug concentrations (50 mu M). Our data demonstrate that arctigenin inhibits iNOS expression via suppressing JAK-STAT signaling pathway in macrophages. Crown Copyright (C) 2011 Published by Elsevier B.V. All rights reserved.
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