16α,17α-epoxypregnenolone-20-oxime prevent LPS-induced NO production and iNOS expression in BV-2 microglial cells by inhibiting JNK phosphorylation

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dc.contributor.authorH N Sun-
dc.contributor.authorM H Jin-
dc.contributor.authorB Han-
dc.contributor.authorL Feng-
dc.contributor.authorY H Han-
dc.contributor.authorG N Shen-
dc.contributor.authorY Z Yu-
dc.contributor.authorC H Jin-
dc.contributor.authorZ X Lian-
dc.contributor.authorD S Lee-
dc.contributor.authorSun-Uk Kim-
dc.contributor.authorW Z Ge-
dc.contributor.authorY D Cui-
dc.date.accessioned2017-04-19T09:55:30Z-
dc.date.available2017-04-19T09:55:30Z-
dc.date.issued2014-
dc.identifier.issn0918-6158-
dc.identifier.uri10.1248/bpb.b13-00706ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/12123-
dc.description.abstractThe free radical nitric oxide (NO), a main member of neuroinflammatory cytokine and a gaseous molecule produced by activated microglia, has many physiological functions, including neuroinflammation. In the present study, we evaluated the effects of serial 16-dehydropregnenolone-3-acetate derivatives on lipopolysaccharide (LPS)-induced NO production and inducible nitric oxide synthase (iNOS) expression in BV-2 microglial cells. Among the six derivatives tested, the increases in NO production and iNOS expression observed in BV-2 microglial cells after LPS stimulation were significantly inhibited by treatment with 16α, 17α-epoxypregnenolone-20-oxime. Moreover, the inhibitory effect of 16α,17α-epoxypregnenolone-20-oxime on NO production was similar to that of S-methylisothiourea sulfate (SMT), an iNOS inhibitor. Further studies showed that 16α,17α-epoxypregnenolone-20-oxime inhibited c-Jun N-terminal kinase (JNK) phosphorylation but not inhibitor kappa B (IκB)-α degradation. Our data in LPS-stimulated microglia cells suggest that 16α,17α-epoxypregnenolone-20-oxime might be a candidate therapeutic for treatment of NO induced neuroinflammation and could be a novel iNOS inhibitor.-
dc.publisherPharmaceutical Soc Japan-
dc.title16α,17α-epoxypregnenolone-20-oxime prevent LPS-induced NO production and iNOS expression in BV-2 microglial cells by inhibiting JNK phosphorylation-
dc.title.alternative16α,17α-epoxypregnenolone-20-oxime prevent LPS-induced NO production and iNOS expression in BV-2 microglial cells by inhibiting JNK phosphorylation-
dc.typeArticle-
dc.citation.titleBiological & Pharmaceutical Bulletin-
dc.citation.number7-
dc.citation.endPage1102-
dc.citation.startPage1096-
dc.citation.volume37-
dc.contributor.affiliatedAuthorSun-Uk Kim-
dc.contributor.alternativeNameSun-
dc.contributor.alternativeNameJin-
dc.contributor.alternativeNameHan-
dc.contributor.alternativeNameFeng-
dc.contributor.alternativeNameHan-
dc.contributor.alternativeNameShen-
dc.contributor.alternativeNameYu-
dc.contributor.alternativeNameJin-
dc.contributor.alternativeNameLian-
dc.contributor.alternativeName이동석-
dc.contributor.alternativeName김선욱-
dc.contributor.alternativeNameGe-
dc.contributor.alternativeNameCui-
dc.identifier.bibliographicCitationBiological & Pharmaceutical Bulletin, vol. 37, no. 7, pp. 1096-1102-
dc.identifier.doi10.1248/bpb.b13-00706-
dc.subject.keywordMicroglia-
dc.subject.keywordNeuroinflammation-
dc.subject.keywordNitric oxide-
dc.subject.localmicroglia-
dc.subject.localMicroglia-
dc.subject.localneuroinflammation-
dc.subject.localNeuroinflammation-
dc.subject.localNO-
dc.subject.localnitric oxide-
dc.subject.localnitric oxide (NO)-
dc.subject.localNitric oxide-
dc.subject.localNO (Nitric oxide)-
dc.subject.localnitric oxide.-
dc.subject.localNitric oxid-
dc.subject.localNitric oxide (NO)-
dc.description.journalClassY-
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Ochang Branch Institute > Division of National Bio-Infrastructure > Futuristic Animal Resource & Research Center > 1. Journal Articles
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