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Mediators of Inflammation
Volume 2010, Article ID 194896, 8 pages
http://dx.doi.org/10.1155/2010/194896
Research Article

Rhizoma coptidis Inhibits LPS-Induced MCP-1/CCL2 Production in Murine Macrophages via an AP-1 and NF B-Dependent Pathway

1Medizinische Klinik III, Universität Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany
2Deutsche Gesellschaft für Traditionelle Chinesische Medizin (DGTCM), 69126 Heidelberg, Germany
3Institute of Biomedical Sciences Abel Salazar, Porto University, 4099-002 Porto, Portugal
4Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA 98195-7234, USA
5Medizinische Klinik IV, Universität Heidelberg, 69120 Heidlberg, Germany

Received 3 December 2009; Revised 18 April 2010; Accepted 7 May 2010

Academic Editor: Giuseppe Valacchi

Copyright © 2010 Andrew Remppis et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Introduction. The Chinese extract Rhizoma coptidis is well known for its anti-inflammatory, antioxidative, antiviral, and antimicrobial activity. The exact mechanisms of action are not fully understood. Methods. We examined the effect of the extract and its main compound, berberine, on LPS-induced inflammatory activity in a murine macrophage cell line. RAW 264.7 cells were stimulated with LPS and incubated with either Rhizoma coptidis extract or berberine. Activation of AP-1 and NF B was analyzed in nuclear extracts, secretion of MCP-1/CCL2 was measured in supernatants. Results. Incubation with Rhizoma coptidis and berberine strongly inhibited LPS-induced monocyte chemoattractant protein (MCP)-1 production in RAW cells. Activation of the transcription factors AP-1 and NF B was inhibited by Rhizoma coptidis in a dose- and time-dependent fashion. Conclusions. Rhizoma coptidis extract inhibits LPS-induced MCP-1/CCL2 production in vitro via an AP-1 and NF B-dependent pathway. Anti-inflammatory action of the extract is mediated mainly by its alkaloid compound berberine.