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dc.contributor.authorZhou, H.
dc.contributor.authorYang, R.
dc.contributor.authorWang, W.
dc.date.accessioned2019-06-05T18:28:19Z
dc.date.available2019-06-05T18:28:19Z
dc.date.issued2018
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85050812166&doi=10.1038%2fs41598-018-29491-7&partnerID=40&md5=a160aa9abcc500bfb1f98dec97ccc6ef
dc.identifier.urihttp://hdl.handle.net/10713/9455
dc.description.abstractApelin is a peptide hormone with anti-oxidative and anti-inflammatory activities and is proposed to be a potential therapeutic for many disease conditions, including sepsis. However, short in vivo half-life of the apelin peptide would limit its potential clinical applications. This study aims to investigate the effects of Fc-apelin, a novel long-acting apelin fusion protein, on lipopolysaccharide (LPS)-induced liver injury. Liver injury was induced by systemic injection of LPS in mice. Hepatoprotective activities of Fc-apelin against inflammation were evaluated in LPS mice and/or hepatoma Huh-7 cells with respect to serum ALT, apoptosis, oxidative stress, macrophage infiltration and gene expression. We found that LPS induced systemic inflammation and liver damage. Co-administration of Fc-apelin significantly attenuated serum ALT elevation, diminished LPS-induced apoptosis and ROS production in the liver and in Huh-7 cells, mitigated hepatic macrophage infiltration, and reduced TNFα and IL-6 gene expression. Collectively, Fc-apelin fusion protein exerts protective effects against LPS-induced liver damage and may serve as a potential therapeutic for endotoxin-induced liver injury. Copyright 2018, The Author(s).en_US
dc.description.urihttps://dx.doi.org/10.1038/s41598-018-29491-7en_US
dc.language.isoen-USen_US
dc.publisherNature Publishing Groupen_US
dc.relation.ispartofScientific Reports
dc.subjectFc-apelin fusion proteinen_US
dc.subject.meshInflammation Mediatorsen_US
dc.subject.meshLiver--pathologyen_US
dc.titleFc-apelin fusion protein attenuates lipopolysaccharide-induced liver injury in miceen_US
dc.typeArticleen_US
dc.identifier.doi10.1038/s41598-018-29491-7
dc.identifier.pmid30061611


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