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

Ethnopharmacological relevanceRhizoma 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 studyThis study was designed to assess the beneficial effects of pretreatment with RC in ameliorating LPS-induced liver inflammation.Materials and methodsMice were orally administered RC (500, 1000 mg/kg) for three days in a row. 1 h 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.ResultsWe 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).ConclusionsThe results presented here clearly demonstrate that RC could significantly protect mice against LPS-induced acute liver injury.

Rhizoma coptidis (RC) suppressed secretion of LPS-stimulated pro-inflammatory cytokines, such as interleukin-6 (IL-6). In addition, RC inhibited LPS-mediated nuclear factor (NF)-κB activation via the prevention of IκB-α phosphorylation, MAPKs phosphorylation, as well as cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (I-NOS).215