2. Academic Validation
  3. Rhizoma Coptidis inhibits LPS-induced MCP-1/CCL2 production in murine macrophages via an AP-1 and NFkappaB-dependent pathway

Rhizoma Coptidis inhibits LPS-induced MCP-1/CCL2 production in murine macrophages via an AP-1 and NFkappaB-dependent pathway

  • Mediators Inflamm. 2010:2010:194896. doi: 10.1155/2010/194896.
Andrew Remppis 1,  Florian Bea,  Henry Johannes Greten,  Annette Buttler,  Hongjie Wang,  Qianxing Zhou,  Michael R Preusch,  Ronny Enk,  Robert Ehehalt,  Hugo Katus,  Erwin Blessing
Affiliations

Affiliation

  • 1 Medizinische Klinik III, Universität Heidelberg, 69120 Heidelberg, Germany.
PMID: 20652055 DOI: 10.1155/2010/194896
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 NFkappaB 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 NFkappaB 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 NFkappaB-dependent pathway. Anti-inflammatory action of the extract is mediated mainly by its alkaloid compound berberine.

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