Inhibitory effect of Coptis chinensis on inflammation in LPS-induced endotoxemia

J Ethnopharmacol. 2013 Sep 16;149(2):506-12. doi: 10.1016/j.jep.2013.07.008. Epub 2013 Jul 18.

Abstract

Ethnopharmacological relevance: Rhizoma coptidis (RC) has been used as a remedy for inflammation-related diseases in traditional medicine. Although it is known to have anti-inflammatory activities, its mechanism of action on lipopolysaccharide (LPS)-induced inflammation has not yet been identified in detail.

Aim of the study: This study was designed to assess the beneficial effects of pretreatment with RC in ameliorating LPS-induced liver inflammation.

Materials and methods: Mice were orally administered RC (500, 1000 mg/kg) for three days in a row. 1h after the last RC administration, the mice were intraperitoneally injected with LPS (35 mg/kg). After treatment, histological alterations and inflammatory factor levels in the liver and proinflammatory cytokines in the serum associated with inflammation were examined.

Results: We found that pretreatment with RC (500 and 1000 mg/kg) exerted a significant protective effect by attenuating liver histopathological changes in endotoxemic mice. The results also demonstrated that RC suppressed secretion of LPS-stimulated pro-inflammatory cytokines, such as interleukin-6 (IL-6). Furthermore, RC inhibited LPS-mediated nuclear factor (NF)-κB activation via the prevention of IκB-α phosphorylation, as well as the phosphorylation of ERK1/2, JNK, and p38 MAPKs. These results were associated with decreases in the expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (I-NOS).

Conclusions: The results presented here clearly demonstrate that RC could significantly protect mice against LPS-induced acute liver injury.

Keywords: Coptis chinensis; IL-6; Lipopolysaccharide (LPS); MAPKs; NF-κB.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology
  • Anti-Inflammatory Agents / therapeutic use*
  • Coptis*
  • Cyclooxygenase 2 / metabolism
  • Endotoxemia / chemically induced
  • Endotoxemia / drug therapy*
  • Endotoxemia / metabolism
  • Endotoxemia / pathology
  • Female
  • Hepatitis / drug therapy*
  • Hepatitis / metabolism
  • Hepatitis / pathology
  • I-kappa B Proteins / metabolism
  • Interferon-gamma / blood
  • Interleukin-6 / blood
  • Lipopolysaccharides
  • Liver / drug effects
  • Liver / metabolism
  • Liver / pathology
  • Mice
  • Mice, Inbred ICR
  • Mitogen-Activated Protein Kinases / metabolism
  • NF-KappaB Inhibitor alpha
  • NF-kappa B / metabolism
  • Nitric Oxide Synthase Type II / metabolism
  • Rhizome

Substances

  • Anti-Inflammatory Agents
  • I-kappa B Proteins
  • Interleukin-6
  • Lipopolysaccharides
  • NF-kappa B
  • Nfkbia protein, mouse
  • NF-KappaB Inhibitor alpha
  • Interferon-gamma
  • Nitric Oxide Synthase Type II
  • Nos2 protein, mouse
  • Ptgs2 protein, mouse
  • Cyclooxygenase 2
  • Mitogen-Activated Protein Kinases