Inhibitory effects of alternaramide on inflammatory mediator expression through TLR4-MyD88-mediated inhibition of NF-kB and MAPK pathway signaling in lipopolysaccharide-stimulated RAW264.7 and BV2 cells

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dc.contributor.authorW Ko-
dc.contributor.authorJ H Sohn-
dc.contributor.authorJae-Hyuk Jang-
dc.contributor.authorJong Seog Ahn-
dc.contributor.authorD G Kang-
dc.contributor.authorH S Lee-
dc.contributor.authorJ S Kim-
dc.contributor.authorY C Kim-
dc.contributor.authorH Oh-
dc.date.accessioned2017-04-19T10:15:31Z-
dc.date.available2017-04-19T10:15:31Z-
dc.date.issued2016-
dc.identifier.issn0009-2797-
dc.identifier.uri10.1016/j.cbi.2015.11.024ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/13033-
dc.description.abstractAlternaramide (1), a novel lipophilic depsipeptide, has been isolated from the extract of the marine-derived fungus Alternaria sp. SF-5016. In the course of extensive biological evaluation of 1, its anti-inflammatory effects in lipopolysaccharide (LPS)-stimulated RAW264.7 and BV2 cells were observed. In our initial study of the anti-inflammatory effects of 1, the compound suppressed production of nitric oxide (NO) and prostaglandin E2 (PGE2) in LPS-stimulated RAW264.7 and BV2 cells. Suppression of NO and PGE2 production was correlated with the inhibitory effect of 1 on expression of LPS-induced inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) at the protein level in RAW264.7 and BV2 cells. In addition, 1 reduced production of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, and IL-12 in LPS-stimulated RAW264.7 and BV2 cells. In the evaluation of the molecular mechanisms underlying the anti-inflammatory effects of 1, the compound was found to suppress the nuclear factor-kappa B (NF-κB) signaling pathway in RAW264.7 and BV2 cells stimulated with LPS. This suppression was mediated by disruption of phosphorylation and degradation of IκBα, an inhibitor of NF-κB, in the cytoplasm, and blocking of nuclear translocation of the NF-κB p50-p65 heterodimer. Furthermore, 1 inhibited phosphorylation of c-Jun N-terminal kinases (JNKs) and p38 mitogen-activated protein kinase (MAPK), demonstrating its capacity to inhibit MAPK signaling. Finally, 1 markedly reduced expression of Toll-like receptor 4 (TLR4) and myeloid differentiation primary response gene 88 (MyD88) at the mRNA and protein levels in LPS-stimulated RAW264.7 and BV2 cells. Taken together, the results of the present study suggest that 1 modulates several TLR4-mediated inflammatory pathways, demonstrating its potential in the treatment of inflammatory and neuroinflammatory conditions.-
dc.publisherElsevier-
dc.titleInhibitory effects of alternaramide on inflammatory mediator expression through TLR4-MyD88-mediated inhibition of NF-kB and MAPK pathway signaling in lipopolysaccharide-stimulated RAW264.7 and BV2 cells-
dc.title.alternativeInhibitory effects of alternaramide on inflammatory mediator expression through TLR4-MyD88-mediated inhibition of NF-kB and MAPK pathway signaling in lipopolysaccharide-stimulated RAW264.7 and BV2 cells-
dc.typeArticle-
dc.citation.titleChemico-Biological Interactions-
dc.citation.number0-
dc.citation.endPage26-
dc.citation.startPage16-
dc.citation.volume244-
dc.contributor.affiliatedAuthorJae-Hyuk Jang-
dc.contributor.affiliatedAuthorJong Seog Ahn-
dc.contributor.alternativeName고원민-
dc.contributor.alternativeName손재학-
dc.contributor.alternativeName장재혁-
dc.contributor.alternativeName안종석-
dc.contributor.alternativeName강대길-
dc.contributor.alternativeName이호섭-
dc.contributor.alternativeName김종수-
dc.contributor.alternativeName김연철-
dc.contributor.alternativeName오현철-
dc.identifier.bibliographicCitationChemico-Biological Interactions, vol. 244, pp. 16-26-
dc.identifier.doi10.1016/j.cbi.2015.11.024-
dc.subject.keywordAlternaramide-
dc.subject.keywordAnti-inflammation-
dc.subject.keywordMAPK-
dc.subject.keywordMarine-derived fungus-
dc.subject.keywordNuclear factor-kappa B-
dc.subject.keywordToll-like receptor 4-
dc.subject.localAlternaramide-
dc.subject.localantiinflammation-
dc.subject.localAntiinflammation-
dc.subject.localanti-inflammation-
dc.subject.localAnti-Inflammation-
dc.subject.localAnti-inflammation-
dc.subject.localMAPK-
dc.subject.localMAPKs-
dc.subject.localmarine-derived fungus-
dc.subject.localMarine-derived fungus-
dc.subject.localNuclear factor-kappa B-
dc.subject.localnuclear factor κB-
dc.subject.localNf-κb-
dc.subject.localNF-kB-
dc.subject.localnuclear factor kappa B-
dc.subject.localNF-κB (nuclear factor kappa-B)-
dc.subject.localNF-kappaB-
dc.subject.localNuclear factor-κb-
dc.subject.localNF-κ B-
dc.subject.localNF-κB-
dc.subject.localNF-kappa B-
dc.subject.localNuclear factor κB (NF-κB)-
dc.subject.localNuclear factor κB-
dc.subject.localNFκB-
dc.subject.localNf-κB-
dc.subject.localNuclear factor-κB-
dc.subject.localnuclear factorκB-
dc.subject.localNuclear factor (NF)-κB-
dc.subject.localNuclear factor kappa B-
dc.subject.localnuclear factor-κB-
dc.subject.localNF-ΚB-
dc.subject.localNuclear factor-kappa B (NF-κB)-
dc.subject.localNuclear factor-kappaB-
dc.subject.localnuclear factor-kappaB-
dc.subject.localnuclear factor-kappaB (NF-κB)-
dc.subject.localNFkappaB-
dc.subject.localNuclear factor kappaB-
dc.subject.localToll-like receptor 4-
dc.subject.localToll-like-receptor4-
dc.subject.localToll-like receptor 4 (TLR4)-
dc.subject.localTLR4-
dc.description.journalClassY-
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