Anti-infammatory efect of hispidin on LPS induced macrophage infammation through MAPK and JAK1/STAT3 signaling pathways

Cited 19 time in scopus
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dc.contributor.authorY H Han-
dc.contributor.authorD Q Chen-
dc.contributor.authorM H Jin-
dc.contributor.authorY H Jin-
dc.contributor.authorJ Li-
dc.contributor.authorG N Shen-
dc.contributor.authorW L Li-
dc.contributor.authorY X Gong-
dc.contributor.authorY Y Mao-
dc.contributor.authorD P Xie-
dc.contributor.authorD S Lee-
dc.contributor.authorL Y Yu-
dc.contributor.authorSun-Uk Kim-
dc.contributor.authorJi-Su Kim-
dc.contributor.authorTaeho Kwon-
dc.contributor.authorY D Cui-
dc.contributor.authorH N Sun-
dc.date.accessioned2020-08-25T10:02:15Z-
dc.date.available2020-08-25T10:02:15Z-
dc.date.issued2020-
dc.identifier.issn2468-0834-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/20127-
dc.description.abstractSevere inflammatory reactions caused by macrophage activation can trigger a systemic immune response. In the present study, we observed the anti-inflammatory properties of hispidin on LPS induced RAW264.7 macrophage cells. Our results showed that hispidin treatment significantly reduced the production of cellular NO, IL-6 and reactive oxygen species (ROS) while has not inhibitory effect on TNF-α productions. Excitingly, hispidin treatment retains the phagocytosis ability of macrophages which enabling them to perform the function of removing foreign invaders. Signaling studies showed, hispidin treatment dramatic suppressed the LPS induced mitogen activated protein kinases (MAPK) and JAK/STAT activations. In conclusion, our findings suggest that hispidin may be a new therapeutic target for clinical treatment of macrophages-mediated inflammatory responses.-
dc.publisherSpringer-
dc.titleAnti-infammatory efect of hispidin on LPS induced macrophage infammation through MAPK and JAK1/STAT3 signaling pathways-
dc.title.alternativeAnti-infammatory efect of hispidin on LPS induced macrophage infammation through MAPK and JAK1/STAT3 signaling pathways-
dc.typeArticle-
dc.citation.titleApplied Biological Chemistry-
dc.citation.number0-
dc.citation.endPage21-
dc.citation.startPage21-
dc.citation.volume63-
dc.contributor.affiliatedAuthorSun-Uk Kim-
dc.contributor.affiliatedAuthorJi-Su Kim-
dc.contributor.affiliatedAuthorTaeho Kwon-
dc.contributor.alternativeNameHan-
dc.contributor.alternativeNameChen-
dc.contributor.alternativeNameJin-
dc.contributor.alternativeNameJin-
dc.contributor.alternativeNameLi-
dc.contributor.alternativeNameShen-
dc.contributor.alternativeNameLi-
dc.contributor.alternativeNameGong-
dc.contributor.alternativeNameMao-
dc.contributor.alternativeNameXie-
dc.contributor.alternativeName이동석-
dc.contributor.alternativeNameYu-
dc.contributor.alternativeName김선욱-
dc.contributor.alternativeName김지수-
dc.contributor.alternativeName권태호-
dc.contributor.alternativeNameCui-
dc.contributor.alternativeNameSun-
dc.identifier.bibliographicCitationApplied Biological Chemistry, vol. 63, pp. 21-21-
dc.identifier.doi10.1186/s13765-020-00504-2-
dc.subject.keywordHispidin-
dc.subject.keywordLPS-
dc.subject.keywordMacrophage-
dc.subject.keywordROS-
dc.subject.keywordSignal transduction-
dc.subject.localHispidin-
dc.subject.localhispidin-
dc.subject.localLPS-
dc.subject.localmacrophages-
dc.subject.localmacrophage-
dc.subject.localMacrophages-
dc.subject.localMacrophage-
dc.subject.localReactive oxidative species-
dc.subject.localReactive oxygen species(ROS)-
dc.subject.localReactive oxygen species-
dc.subject.localReactive Oxygen Species (ROS)-
dc.subject.localReactive Oxygen Species-
dc.subject.localROS-
dc.subject.localReactive oxygen species (ROS)-
dc.subject.localreactive oxygen species-
dc.subject.localreactive oxygen species (ROS)-
dc.subject.localSignal transduction-
dc.subject.localSignal trasduction-
dc.subject.localsignal transduction-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Division of National Bio-Infrastructure > Futuristic Animal Resource & Research Center > 1. Journal Articles
Jeonbuk Branch Institute > Primate Resources Center > 1. Journal Articles
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