DC Field | Value | Language |
---|---|---|
dc.contributor.author | W Ko | - |
dc.contributor.author | J H Sohn | - |
dc.contributor.author | Jae-Hyuk Jang | - |
dc.contributor.author | Jong Seog Ahn | - |
dc.contributor.author | D G Kang | - |
dc.contributor.author | H S Lee | - |
dc.contributor.author | J S Kim | - |
dc.contributor.author | Y C Kim | - |
dc.contributor.author | H Oh | - |
dc.date.accessioned | 2017-04-19T10:15:31Z | - |
dc.date.available | 2017-04-19T10:15:31Z | - |
dc.date.issued | 2016 | - |
dc.identifier.issn | 0009-2797 | - |
dc.identifier.uri | 10.1016/j.cbi.2015.11.024 | ko |
dc.identifier.uri | https://oak.kribb.re.kr/handle/201005/13033 | - |
dc.description.abstract | Alternaramide (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.publisher | Elsevier | - |
dc.title | 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 | - |
dc.title.alternative | 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 | - |
dc.type | Article | - |
dc.citation.title | Chemico-Biological Interactions | - |
dc.citation.number | 0 | - |
dc.citation.endPage | 26 | - |
dc.citation.startPage | 16 | - |
dc.citation.volume | 244 | - |
dc.contributor.affiliatedAuthor | Jae-Hyuk Jang | - |
dc.contributor.affiliatedAuthor | Jong Seog Ahn | - |
dc.contributor.alternativeName | 고원민 | - |
dc.contributor.alternativeName | 손재학 | - |
dc.contributor.alternativeName | 장재혁 | - |
dc.contributor.alternativeName | 안종석 | - |
dc.contributor.alternativeName | 강대길 | - |
dc.contributor.alternativeName | 이호섭 | - |
dc.contributor.alternativeName | 김종수 | - |
dc.contributor.alternativeName | 김연철 | - |
dc.contributor.alternativeName | 오현철 | - |
dc.identifier.bibliographicCitation | Chemico-Biological Interactions, vol. 244, pp. 16-26 | - |
dc.identifier.doi | 10.1016/j.cbi.2015.11.024 | - |
dc.subject.keyword | Alternaramide | - |
dc.subject.keyword | Anti-inflammation | - |
dc.subject.keyword | MAPK | - |
dc.subject.keyword | Marine-derived fungus | - |
dc.subject.keyword | Nuclear factor-kappa B | - |
dc.subject.keyword | Toll-like receptor 4 | - |
dc.subject.local | Alternaramide | - |
dc.subject.local | antiinflammation | - |
dc.subject.local | Antiinflammation | - |
dc.subject.local | anti-inflammation | - |
dc.subject.local | Anti-Inflammation | - |
dc.subject.local | Anti-inflammation | - |
dc.subject.local | MAPK | - |
dc.subject.local | MAPKs | - |
dc.subject.local | marine-derived fungus | - |
dc.subject.local | Marine-derived fungus | - |
dc.subject.local | Nuclear factor-kappa B | - |
dc.subject.local | nuclear factor κB | - |
dc.subject.local | Nf-κb | - |
dc.subject.local | NF-kB | - |
dc.subject.local | nuclear factor kappa B | - |
dc.subject.local | NF-κB (nuclear factor kappa-B) | - |
dc.subject.local | NF-kappaB | - |
dc.subject.local | Nuclear factor-κb | - |
dc.subject.local | NF-κ B | - |
dc.subject.local | NF-κB | - |
dc.subject.local | NF-kappa B | - |
dc.subject.local | Nuclear factor κB (NF-κB) | - |
dc.subject.local | Nuclear factor κB | - |
dc.subject.local | NFκB | - |
dc.subject.local | Nf-κB | - |
dc.subject.local | Nuclear factor-κB | - |
dc.subject.local | nuclear factorκB | - |
dc.subject.local | Nuclear factor (NF)-κB | - |
dc.subject.local | Nuclear factor kappa B | - |
dc.subject.local | nuclear factor-κB | - |
dc.subject.local | NF-ΚB | - |
dc.subject.local | Nuclear factor-kappa B (NF-κB) | - |
dc.subject.local | Nuclear factor-kappaB | - |
dc.subject.local | nuclear factor-kappaB | - |
dc.subject.local | nuclear factor-kappaB (NF-κB) | - |
dc.subject.local | NFkappaB | - |
dc.subject.local | Nuclear factor kappaB | - |
dc.subject.local | Toll-like receptor 4 | - |
dc.subject.local | Toll-like-receptor4 | - |
dc.subject.local | Toll-like receptor 4 (TLR4) | - |
dc.subject.local | TLR4 | - |
dc.description.journalClass | Y | - |
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