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Cho, Young-Chang,Lee, In-Seon,Seo, Huiyun,Ju, Anna,Youn, Deokkyu,Kim, Younghyun,Choun, Jaehee,Cho, Sayeon SPANDIDOS PUBLICATIONS 2014 MOLECULAR MEDICINE REPORTS Vol.10 No.5
<P>Numerous Euphorbiaceae plants have been used for the treatment of diseases, including liver diseases, asthma and rheumatism. The present study evaluated the effect of methanol extracts from Euphorbia cooperi (MEC), a member of the Euphorbiaceae plant family, on the production of inflammatory cytokines interleukin (IL)?6 and tumor necrosis factor (TNF)?α, nitric oxide (NO) as well as the activation of mitogen?activated protein kinase and nuclear factor (NF)?κB signaling. Non?cytotoxic concentrations of MEC significantly reduced the production of NO and IL?6, but not TNF?α, in lipopolysaccharide (LPS)?stimulated RAW 264.7 macrophages. The decreased production of NO by MEC was due to alleviated expression of inducible NO synthase. Reporter assays with cells treated with MEC demonstrated reduced activator protein?1 (AP-1) activity, while NF?κB activity was not reduced. Furthermore, the phosphorylation levels of c?Jun N?terminal kinase (JNK) and p38 were suppressed by MEC while phosphorylation levels of inhibitor of κB were not reduced by MEC, suggesting that MEC?mediated inactivation of JNK and p38 is the underlying regulatory mechanism for inflammatory mediators in LPS?stimulated RAW 264.7 macrophages.</P>
Young-Chang Cho,Jaehee Choun Sayeon Cho 한국구조생물학회 2014 Biodesign Vol.2 No.3
Many attempts have been made to develop anti-inflammatory drugs by using natural products because natural products have been traditionally used to cure severe inflammatory diseases. In this study, we investigated the anti-inflammatory effects and the molecular mechanisms underlying these effects in murine macrophages by using an ethanol extract of Callicarpa 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 levels of inducible nitric oxide synthase (iNOS). However, ECR did not modulate cyclooxygenase-2 (COX-2) expression at both mRNA and protein levels. Among the inflammatory cytokines, interleukin (IL)-1β production was reduced by ECR treatment whereas the level of IL-6 and tumor necrosis factor (TNF)-α was independent of ECR treatment. Western blot analysis revealed that ECR notably reduced the phosphorylation of p38 but had no effect on the activation of nuclear factor kappa B (NF-κB) and other mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK). These results imply that ECR exerts anti-inflammatory effects via selective inhibition of the production of inflammatory mediators including iNOS and IL-1β by inactivating p38.