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dc.contributor.author전대원-
dc.date.accessioned2019-12-03T04:19:17Z-
dc.date.available2019-12-03T04:19:17Z-
dc.date.issued2017-12-
dc.identifier.citationONCOTARGET, v. 8, no. 58, page. 97965-97976en_US
dc.identifier.issn1949-2553-
dc.identifier.urihttp://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=view&path[]=18967&path[]=60800-
dc.identifier.urihttp://repository.hanyang.ac.kr/handle/20.500.11754/116757-
dc.description.abstractProtective effects of granulocyte colony stimulating factor (G-CSF) in acute liver injury via marrow cell mobilization have been reported in several studies. But exact mode of action and optimal protocol of G-CSF has been still doubt in chronic disease. Here we investigated mode of action and optimization of G-CSF as a treatment for nonalcoholic fatty liver disease (NAFLD). Various doses of conventional G-CSF (30 mu g/kg once weekly, once daily for 5 days, twice weekly) and long acting G-CSF (30 mu g/kg once a month) were evaluated in two kinds of NAFLD animal models to optimize the G-CSF protocol. G-CSF receptor expression highest increased in NAFLD model among various liver diseases compare to control (NAFLD: 14.7 times, alcohol hepatitis: 7.1 times, cirrhosis: 2.4 times, and ischemia reperfusion: 6.8 times). G-CSF treatment reduced intrahepatic fat accumulation, and inflammation in two kinds of NAFLD animal models. G-CSF increased PI3K/Akt expression in hepatocyte as well as decreased apoptotic drive (increased Bcl-2 expression and decreased Bax expression) in animal model. Five day consecutive G-CSF treatment and once a month long acting G-CSF increased marrow derived stem cell marker in peripheral blood. But twice a week conventional G-CSF treatment did not increased CD34+ cell in peripheral blood and liver neither. Not only high dose G-CSF (once daily for 5 days) but also hepatotropic dose G-CSF (twice a week) significantly reduced hepatocyte apoptosis via PI3K and Akt pathway activation without marrow cell mobilization in NAFLD animal model.en_US
dc.description.sponsorshipThis work was supported by a grant from National Research Foundation of Korea 2011-0007127.en_US
dc.language.isoen_USen_US
dc.publisherIMPACT JOURNALS LLCen_US
dc.subjectnon-alcoholic fatty liveren_US
dc.subjectgranulocyte colony stimulating factoren_US
dc.subjectapoptosisen_US
dc.titleGranulocyte colony stimulating factor treatment in non-alcoholic fatty liver disease: Beyond marrow cell mobilizationen_US
dc.typeArticleen_US
dc.relation.no58-
dc.relation.volume8-
dc.identifier.doi10.18632/oncotarget.18967-
dc.relation.page97965-97976-
dc.relation.journalONCOTARGET-
dc.contributor.googleauthorNam, Ho Hyun-
dc.contributor.googleauthorJun, Dae Won-
dc.contributor.googleauthorJang, Kiseok-
dc.contributor.googleauthorSaeed, Waqar Khalid-
dc.contributor.googleauthorLee, Jai Sun-
dc.contributor.googleauthorKang, Hyeon Tae-
dc.contributor.googleauthorChae, Yeon Ji-
dc.relation.code2017009424-
dc.sector.campusS-
dc.sector.daehakCOLLEGE OF MEDICINE[S]-
dc.sector.departmentDEPARTMENT OF MEDICINE-
dc.identifier.pidnoshin-


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