Callicarpa rubella for. angustata C. P’ei shows anti-inflammatory effects by blocking p38 activation in murine macrophages

Abstract

Many attempts have been made to develop anti-inflammatory drugs by using natural products because natural productshave been traditionally used to cure severe inflammatory diseases. In this study, we investigated the anti-inflammatoryeffects and the molecular mechanisms underlying these effects in murine macrophages by using an ethanol extract ofCallicarpa rubella for. angustata C. P`ei (ECR). We found that ECR treatment significantly inhibited lipopolysaccharide(LPS)-stimulated nitric oxide (NO) production in macrophages and downregulated mRNA and protein expression levelsof inducible nitric oxide synthase (iNOS). However, ECR did not modulate cyclooxygenase-2 (COX-2) expression at bothmRNA and protein levels. Among the inflammatory cytokines, interleukin (IL)-1β production was reduced by ECR treatmentwhereas the level of IL-6 and tumor necrosis factor (TNF)-α was independent of ECR treatment. Western blot analysisrevealed that ECR notably reduced the phosphorylation of p38 but had no effect on the activation of nuclear factor kappaB (NF-κB) and other mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinase (ERK) andc-Jun N-terminal kinase (JNK). These results imply that ECR exerts anti-inflammatory effects via selective inhibition of theproduction of inflammatory mediators including iNOS and IL-1β by inactivating p38.