Longifolioside A inhibits TLR4-mediated inflammatory responses by blocking PKCδ activation in LPS-stimulated THP-1 macrophages

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dc.contributor.authorSu Ui Lee-
dc.contributor.authorEun Sol Oh-
dc.contributor.authorHyung Won Ryu-
dc.contributor.authorMun-Ock Kim-
dc.contributor.authorMyung Ji Kang-
dc.contributor.authorYu Na Song-
dc.contributor.authorRo Woon Lee-
dc.contributor.authorDoo-Young Kim-
dc.contributor.authorH Ro-
dc.contributor.authorSunin Jung-
dc.contributor.authorS T Hong-
dc.contributor.authorSei-Ryang Oh-
dc.date.accessioned2020-09-24T03:09:54Z-
dc.date.available2020-09-24T03:09:54Z-
dc.date.issued2020-
dc.identifier.issn1043-4666-
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/22642-
dc.description.abstractLongifolioside A is an iridoid glucoside compound isolated from Pseudolysimachion rotundum var. subintegrum, which has been used in traditional herbal medicines to treat respiratory inflammatory diseases. Logifolioside A is a potent antioxidant; however, its underlying pharmacological mechanisms of action in inflammatory diseases are unknown. Here, we investigated the inhibitory effects of longifolioside A in lipopolysaccharide (LPS)-stimulated toll-like receptor 4 (TLR4) signal transduction systems using human THP-1 macrophages and HEK293 cells stably expressing human TLR4 protein (293/HA-hTLR4). Longifolioside A significantly reduced the release of inflammatory cytokines such as interleukin (IL)-6, -8, and tumor necrosis factor (TNF)-α in LPS-stimulated THP-1 macrophages. Furthermore, longifolioside A inhibited the expression of inflammatory mediator genes such as inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 that produce nitric oxide (NO) and prostaglandin E2 (PGE2), respectively. Longifolioside A suppressed the phosphorylation of PKCδ, IRAK4, IKKα/β, IκBα, and mitogen-activated protein (MAP) kinases (ERK 1/2 and JNK, but not p38), thereby inactivating the nuclear localization of NF-κB and AP-1, and thus decreasing the expression of inflammatory response genes. Notably, longifolioside A disrupted the interaction between human TLR4 and the TIR domain-containing adaptor protein (TIRAP), an early step during TLR4 activation, thereby reducing IL-8 secretion in 293/HA-hTLR4 cells. This inhibitory effect was comparable to that of TAK-242 (a TLR4 inhibitor, or resatorvid). Our results indicate that longifolioside A prevents inflammatory response by suppressing TLR4 activation required for NF-κB and AP-1 activation.-
dc.publisherElsevier-
dc.titleLongifolioside A inhibits TLR4-mediated inflammatory responses by blocking PKCδ activation in LPS-stimulated THP-1 macrophages-
dc.title.alternativeLongifolioside A inhibits TLR4-mediated inflammatory responses by blocking PKCδ activation in LPS-stimulated THP-1 macrophages-
dc.typeArticle-
dc.citation.titleCytokine-
dc.citation.number0-
dc.citation.endPage155116-
dc.citation.startPage155116-
dc.citation.volume131-
dc.contributor.affiliatedAuthorSu Ui Lee-
dc.contributor.affiliatedAuthorEun Sol Oh-
dc.contributor.affiliatedAuthorHyung Won Ryu-
dc.contributor.affiliatedAuthorMun-Ock Kim-
dc.contributor.affiliatedAuthorMyung Ji Kang-
dc.contributor.affiliatedAuthorYu Na Song-
dc.contributor.affiliatedAuthorRo Woon Lee-
dc.contributor.affiliatedAuthorDoo-Young Kim-
dc.contributor.affiliatedAuthorSunin Jung-
dc.contributor.affiliatedAuthorSei-Ryang Oh-
dc.contributor.alternativeName이수의-
dc.contributor.alternativeName오은솔-
dc.contributor.alternativeName류형원-
dc.contributor.alternativeName김문옥-
dc.contributor.alternativeName강명지-
dc.contributor.alternativeName송유나-
dc.contributor.alternativeName이로운-
dc.contributor.alternativeName김두영-
dc.contributor.alternativeName노현주-
dc.contributor.alternativeName정선인-
dc.contributor.alternativeName홍성태-
dc.contributor.alternativeName오세량-
dc.identifier.bibliographicCitationCytokine, vol. 131, pp. 155116-155116-
dc.identifier.doi10.1016/j.cyto.2020.155116-
dc.subject.keywordInflammation-
dc.subject.keywordLipopolysaccharides-
dc.subject.keywordLongifolioside A-
dc.subject.keywordToll-like receptor 4-
dc.subject.keywordToll/interleukin-1 receptor domain-containing adapter protein-
dc.subject.localInflammation-
dc.subject.localinflammation-
dc.subject.localnflammation-
dc.subject.localLipopolysaccharide-
dc.subject.localLipopolysaccharide (LPS)-
dc.subject.localLipopolysaccharides-
dc.subject.locallipopolysaccharide-
dc.subject.locallipopolysaccharide (LPS)-
dc.subject.localLongifolioside A-
dc.subject.localTLR4-
dc.subject.localToll-like receptor 4-
dc.subject.localToll-like receptor 4 (TLR4)-
dc.subject.localToll-like-receptor4-
dc.subject.localToll/interleukin-1 receptor domain-containing adapter protein-
dc.description.journalClassY-
Appears in Collections:
Ochang Branch Institute > Natural Product Research Center > 1. Journal Articles
Ochang Branch Institute > Division of National Bio-Infrastructure > Bio-Resource Central Bank > 1. Journal Articles
Ochang Branch Institute > 1. Journal Articles
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