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dc.contributor.authorFranceschelli, Saraes_ES
dc.contributor.authorPesce, Mirkoes_ES
dc.contributor.authorFerrone, Alessioes_ES
dc.contributor.authorGatta, Daniela Maria Piaes_ES
dc.contributor.authorPatruno, Antoniaes_ES
dc.contributor.authorLutiis, Maria Anna Dees_ES
dc.contributor.authorQuiles Morales, José Luis es_ES
dc.contributor.authorGrilli, Alfredoes_ES
dc.contributor.authorFelaco, Marioes_ES
dc.contributor.authorSperanza, Lorenzaes_ES
dc.date.accessioned2018-01-23T13:54:33Z
dc.date.available2018-01-23T13:54:33Z
dc.date.issued2017-03-23
dc.identifier.citationFranceschelli, S.; et al. Biological Effect of Licochalcone C on the Regulation of PI3K/Akt/eNOS and NF-κB/iNOS/NO Signaling Pathways in H9c2 Cells in Response to LPS Stimulation. International Journal of Molecular Sciences, 18(4): 690 (2017). [http://hdl.handle.net/10481/49125]es_ES
dc.identifier.issn1422-0067
dc.identifier.urihttp://hdl.handle.net/10481/49125
dc.description.abstractPolyphenols compounds are a group molecules present in many plants. They have antioxidant properties and can also be helpful in the management of sepsis. Licochalcone C (LicoC), a constituent of Glycyrrhiza glabra, has various biological and pharmacological properties. In saying this, the effect of LicoC on the inflammatory response that characterizes septic myocardial dysfunction is poorly understood. The aim of this study was to determine whether LicoC exhibits anti-inflammatory properties on H9c2 cells that are stimulated with lipopolysaccharide. Our results have shown that LicoC treatment represses nuclear factor-κB (NF-κB) translocation and several downstream molecules, such as inducible nitric oxide synthase (iNOS), intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). Moreover, LicoC has upregulated the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/endothelial nitric oxide synthase (eNOS) signaling pathway. Finally, 2-(4-Morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride (LY294002), a specific PI3K inhibitor, blocked the protective effects of LicoC. These findings indicate that LicoC plays a pivotal role in cardiac dysfunction in sepsis-induced inflammation.en_EN
dc.description.sponsorshipThe Italian Ministry for University and Research is acknowledged for financial support.en_EN
dc.language.isoenges_ES
dc.publisherMDPIes_ES
dc.rightsCreative Commons Attribution-NonCommercial-NoDerivs 3.0 Licensees_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/3.0/es_ES
dc.subjectInflammation en_EN
dc.subjectNitric oxideen_EN
dc.subjectLicochalcone Cen_EN
dc.subjectAdhesion moleculeen_EN
dc.subjectCardiomyocytesen_EN
dc.subjectNuclear factor-κBen_EN
dc.subjectAkten_EN
dc.titleBiological Effect of Licochalcone C on the Regulation of PI3K/Akt/eNOS and NF-κB/iNOS/NO Signaling Pathways in H9c2 Cells in Response to LPS Stimulationen_EN
dc.typeinfo:eu-repo/semantics/articleen_EN
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessen_EN
dc.identifier.doi10.3390/ijms18040690


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