Rhizoma coptidis Inhibits LPS-Induced MCP-1/CCL2 Production in Murine Macrophages via an AP-1 and NF𝜅B-Dependent Pathway
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 i...
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| Format: | Article |
| Language: | English |
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Wiley
2010-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2010/194896 |
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| author | Andrew Remppis Florian Bea Henry Johannes Greten Annette Buttler Hongjie Wang Qianxing Zhou Michael R. Preusch Ronny Enk Robert Ehehalt Hugo Katus Erwin Blessing |
| author_facet | Andrew Remppis Florian Bea Henry Johannes Greten Annette Buttler Hongjie Wang Qianxing Zhou Michael R. Preusch Ronny Enk Robert Ehehalt Hugo Katus Erwin Blessing |
| author_sort | Andrew Remppis |
| collection | DOAJ |
| description | 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 NF𝜅B 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 NFB 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 NFB-dependent pathway. Anti-inflammatory action of the extract is mediated mainly by its alkaloid compound berberine. |
| format | Article |
| id | doaj-art-84da526bf39c4a9299c709fe4db580f2 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2010-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-84da526bf39c4a9299c709fe4db580f22025-08-20T03:37:47ZengWileyMediators of Inflammation0962-93511466-18612010-01-01201010.1155/2010/194896194896Rhizoma coptidis Inhibits LPS-Induced MCP-1/CCL2 Production in Murine Macrophages via an AP-1 and NF𝜅B-Dependent PathwayAndrew Remppis0Florian Bea1Henry Johannes Greten2Annette Buttler3Hongjie Wang4Qianxing Zhou5Michael R. Preusch6Ronny Enk7Robert Ehehalt8Hugo Katus9Erwin Blessing10Medizinische Klinik III, Universität Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, GermanyMedizinische Klinik III, Universität Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, GermanyDeutsche Gesellschaft für Traditionelle Chinesische Medizin (DGTCM), 69126 Heidelberg, GermanyMedizinische Klinik III, Universität Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, GermanyMedizinische Klinik III, Universität Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, GermanyMedizinische Klinik III, Universität Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, GermanyDepartment of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA 98195-7234, USAMedizinische Klinik IV, Universität Heidelberg, 69120 Heidlberg, GermanyMedizinische Klinik IV, Universität Heidelberg, 69120 Heidlberg, GermanyMedizinische Klinik III, Universität Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, GermanyMedizinische Klinik III, Universität Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, GermanyIntroduction. 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 NF𝜅B 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 NFB 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 NFB-dependent pathway. Anti-inflammatory action of the extract is mediated mainly by its alkaloid compound berberine.http://dx.doi.org/10.1155/2010/194896 |
| spellingShingle | Andrew Remppis Florian Bea Henry Johannes Greten Annette Buttler Hongjie Wang Qianxing Zhou Michael R. Preusch Ronny Enk Robert Ehehalt Hugo Katus Erwin Blessing Rhizoma coptidis Inhibits LPS-Induced MCP-1/CCL2 Production in Murine Macrophages via an AP-1 and NF𝜅B-Dependent Pathway Mediators of Inflammation |
| title | Rhizoma coptidis Inhibits LPS-Induced MCP-1/CCL2 Production in Murine Macrophages via an AP-1 and NF𝜅B-Dependent Pathway |
| title_full | Rhizoma coptidis Inhibits LPS-Induced MCP-1/CCL2 Production in Murine Macrophages via an AP-1 and NF𝜅B-Dependent Pathway |
| title_fullStr | Rhizoma coptidis Inhibits LPS-Induced MCP-1/CCL2 Production in Murine Macrophages via an AP-1 and NF𝜅B-Dependent Pathway |
| title_full_unstemmed | Rhizoma coptidis Inhibits LPS-Induced MCP-1/CCL2 Production in Murine Macrophages via an AP-1 and NF𝜅B-Dependent Pathway |
| title_short | Rhizoma coptidis Inhibits LPS-Induced MCP-1/CCL2 Production in Murine Macrophages via an AP-1 and NF𝜅B-Dependent Pathway |
| title_sort | rhizoma coptidis inhibits lps induced mcp 1 ccl2 production in murine macrophages via an ap 1 and nf𝜅b dependent pathway |
| url | http://dx.doi.org/10.1155/2010/194896 |
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