Euphorbia supina inhibits inflammatory mediators in mouse bone marrow-derived mast cells and macrophages

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dc.contributor.authorH S Chae-
dc.contributor.authorHyuk-Hwan Song-
dc.contributor.authorY M Kim-
dc.contributor.authorHyeong Kyu Lee-
dc.contributor.authorSei-Ryang Oh-
dc.contributor.authorY W Chin-
dc.date.accessioned2017-04-19T10:15:25Z-
dc.date.available2017-04-19T10:15:25Z-
dc.date.issued2015-
dc.identifier.issn1567-5769-
dc.identifier.uri10.1016/j.intimp.2015.09.008ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/13015-
dc.description.abstractEuphorbia supina has been traditionally used for the treatment of furuncle and bloody diarrhea relevant to the inflammatory process. It has been proven to have a variety of pharmacological efficacies including antiarthritic, detoxification, hemostatic, and diuretic activities. RAW 264.7 macrophages and bone marrow-derived mast cells (BMMCs) were used to determine the anti-inflammatory and anti-allergic effects of E. supina (ES). NO production was assayed by measuring the nitrite content of the supernatants of cultured RAW 264.7 cells. β-hexosaminidase, a marker of mast cell degranulation, was quantitated by spectrophotometric analysis. ELISA was used for the analysis of interleukin-6 expression, and Western blotting was used to analyze 5-LOX, iNOS, and MAPK activation. The relevant gene expression upon ES treatment was measured by RT-PCR. ES inhibited inducible nitric oxide synthase (iNOS) in RAW 264.7 cells, and IL-6 and LTC4 production in PMA- and A23187-induced BMMCs along with the downregulation of 5-LOX gene expression. Furthermore, in the present study, a decrease in p-ERK, p-JNK, and p-P38 expression, as well as the suppression of degranulation, were observed by treatment with ES. Further in vivo study revealed that ES treatment also remarkably inhibited xylene-induced mouse ear edema and MPO levels in mice ears. This study demonstrates that ES has a potential regulatory effect on the expression of inflammatory mediators through the inhibition of both the phosphorylation of MAPK signaling and the activation of degranulation.-
dc.publisherElsevier-
dc.titleEuphorbia supina inhibits inflammatory mediators in mouse bone marrow-derived mast cells and macrophages-
dc.title.alternativeEuphorbia supina inhibits inflammatory mediators in mouse bone marrow-derived mast cells and macrophages-
dc.typeArticle-
dc.citation.titleInternational Immunopharmacology-
dc.citation.number2-
dc.citation.endPage973-
dc.citation.startPage966-
dc.citation.volume29-
dc.contributor.affiliatedAuthorHyuk-Hwan Song-
dc.contributor.affiliatedAuthorHyeong Kyu Lee-
dc.contributor.affiliatedAuthorSei-Ryang Oh-
dc.contributor.alternativeName채희성-
dc.contributor.alternativeName송혁환-
dc.contributor.alternativeName김영미-
dc.contributor.alternativeName이형규-
dc.contributor.alternativeName오세량-
dc.contributor.alternativeName진영원-
dc.identifier.bibliographicCitationInternational Immunopharmacology, vol. 29, no. 2, pp. 966-973-
dc.identifier.doi10.1016/j.intimp.2015.09.008-
dc.subject.keyword5-Lipoxygenase-
dc.subject.keywordEdema-
dc.subject.keywordEuphorbia supina-
dc.subject.keywordInducible nitric oxide synthase-
dc.subject.keywordInflammation-
dc.subject.keywordInterleukin-6-
dc.subject.local5-Lipoxygenase-
dc.subject.local5-lipoxygenase-
dc.subject.localEdema-
dc.subject.localEuphorbia supina-
dc.subject.localeuphorbia supina-
dc.subject.localInducible nitric oxide synthase-
dc.subject.localInducible nitric oxide synthase (iNOS)-
dc.subject.localInducible nitric oxide synthease (iNOS)-
dc.subject.localINOS-
dc.subject.localiNOS-
dc.subject.localinducible nitric oxide synthase-
dc.subject.localinducible nnitric oxide synthase-
dc.subject.localInflammation-
dc.subject.localinflammation-
dc.subject.localnflammation-
dc.subject.localInterleukin-6-
dc.subject.localInterleukin-6 (IL-6)-
dc.subject.localIL-6-
dc.subject.localIL6-
dc.subject.localIl-6-
dc.subject.localinterleukin-6-
dc.subject.localinterleukin-6 (IL-6)-
dc.subject.localinterukin -6-
dc.description.journalClassY-
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Ochang Branch Institute > 1. Journal Articles
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