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Cordycepin inhibits lipopolysaccharide-induced inflammation by the suppression of NF-κB through Akt and p38 inhibition in RAW 264.7 macrophage cells

DC FieldValueLanguage
dc.contributor.author신동직-
dc.contributor.author장양수-
dc.contributor.author정남식-
dc.contributor.author황기철-
dc.date.accessioned2015-06-10T11:58:19Z-
dc.date.available2015-06-10T11:58:19Z-
dc.date.issued2006-
dc.identifier.issn0014-2999-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/108954-
dc.description.abstractCordyceps militaris, a caterpillar-grown traditional medicinal mushroom, produces an important bioactive compound, cordycepin (3'-deoxyadenosine). Cordycepin is reported to possess many pharmacological activities including immunological stimulating, anti-cancer, anti-virus and anti-infection activities. The molecular mechanisms of cordycepin on pharmacological and biochemical actions of macrophages in inflammation have not been clearly elucidated yet. In the present study, we tested the role of cordycepin on the anti-inflammation cascades in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. In LPS-activated macrophage, nitric oxide (NO) production was inhibited by butanol fraction of C. militaris and the major component of C. militaris butanol faction was identified as cordycepin by high performance liquid chromatography. To investigate the mechanism by which cordycepin inhibits NO production and inducible nitric oxide synthase (iNOS) expression, we examined the activation of Akt and MAP kinases in LPS-activated macrophage. Cordycepin markedly inhibited the phosphorylation of Akt and p38 in dose-dependent manners in LPS-activated macrophage. Moreover, cordycepin suppressed tumor necrosis factor (TNF-alpha) expression, IkappaB alpha phosphorylation, and translocation of nuclear factor-kappaB (NF-kappaB). The expressions of cycloxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) were significantly decreased in RAW 264.7 cell by cordycepin. Taken together, these results suggest that cordycepin inhibits the production of NO production by down-regulation of iNOS and COX-2 gene expression via the suppression of NF-kappaB activation, Akt and p38 phosphorylation. Thus, cordycepin may provide a potential therapeutic approach for inflammation-associated disorders.-
dc.description.statementOfResponsibilityopen-
dc.format.extent192~199-
dc.relation.isPartOfEUROPEAN JOURNAL OF PHARMACOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleCordycepin inhibits lipopolysaccharide-induced inflammation by the suppression of NF-κB through Akt and p38 inhibition in RAW 264.7 macrophage cells-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorHo Gyoung Kim-
dc.contributor.googleauthorBhushan Shrestha-
dc.contributor.googleauthorSo Yeon Lim-
dc.contributor.googleauthorDeok Hyo Yoon-
dc.contributor.googleauthorWoo Chul Chang-
dc.contributor.googleauthorDong-Jik Shin-
dc.contributor.googleauthorSang Kuk Han-
dc.contributor.googleauthorSang Min Park-
dc.contributor.googleauthorJung Hee Park-
dc.contributor.googleauthorHae Il Park-
dc.contributor.googleauthorJae-Mo Sung-
dc.contributor.googleauthorYangsoo Jang-
dc.contributor.googleauthorNamsik Chung-
dc.contributor.googleauthorKi-Chul Hwang-
dc.contributor.googleauthorTae Woong Kim-
dc.identifier.doi10.1016/j.ejphar.2006.06.047-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA03448-
dc.contributor.localIdA03585-
dc.contributor.localIdA04456-
dc.relation.journalcodeJ00842-
dc.identifier.eissn1879-0712-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0014299906006674-
dc.subject.keywordCordyceps militaris-
dc.subject.keywordCordycepin-
dc.subject.keywordMacrophage-
dc.subject.keywordInflammation-
dc.subject.keywordNO production-
dc.subject.keywordLipopolysaccharide (LPS)-
dc.contributor.alternativeNameShin, Dong Jik-
dc.contributor.alternativeNameJang, Yang Soo-
dc.contributor.alternativeNameChung, Nam Sik-
dc.contributor.alternativeNameHwang, Ki Chul-
dc.contributor.affiliatedAuthorJang, Yang Soo-
dc.contributor.affiliatedAuthorChung, Nam Sik-
dc.contributor.affiliatedAuthorHwang, Ki Chul-
dc.rights.accessRightsnot free-
dc.citation.volume545-
dc.citation.number2-3-
dc.citation.startPage192-
dc.citation.endPage199-
dc.identifier.bibliographicCitationEUROPEAN JOURNAL OF PHARMACOLOGY, Vol.545(2-3) : 192-199, 2006-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
5. Research Institutes (연구소) > Research Center for Human Natural Defense System (생체방어연구센터) > 1. Journal Papers
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers

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