Insulin like growth factor-1 increases fatty liver preservation in IGL-1 solution

被引:2
作者
Mohamed Amine Zaouali [1 ,2 ]
Susagna Padrissa-Altés [1 ]
Ismail Ben Mosbah [1 ]
Hassen Ben Abdennebi [3 ]
Olivier Boillot [4 ]
Antoni Rimola [2 ,5 ]
Dalila Saidane-Mosbahi [3 ]
Joan Roselló-Catafau [1 ,2 ,5 ]
机构
[1] Experimental Hepatic Ischemia-Reperfusion Unit,Institut d'Investigacions Biomèdiques de Barcelona,Consejo Superior de Investigaciones Científicas,08036 Barcelona,Spain
[2] Unitat de Transplantament de Fetgei Viabilitat del' Empelt,Institut d'Investigacions Biomèdiques August Pii Sunyer,08036 Barcelona,Spain
[3] Laboratory of Human Physiology,Faculty of Pharmacy,University of Monastir,5000 Monastir,Tunisia
[4] Unit of Hepatic Transplantation,Edouard Herriot Hospital,69003 Lyon,France
[5] Biomedical Research Center Esther Koplowitz,CIBER-ehd,Institute of Health Carlos Ⅲ,08036 Barcelona,Spain
关键词
AKT; Institut georges lopez-1 solution; Insulin like growth factor-1; Ischemia reperfusion injury; Nitric oxide; Oxidative stress; Steatotic graft preservation;
D O I
暂无
中图分类号
R575.5 [肝代谢障碍];
学科分类号
1002 ; 100201 ;
摘要
AIM: To investigate the benefits of insulin like growth factor-1 (IGF-1) supplementation to serum-free institut georges lopez-1 (IGL-1) solution to protect fatty liver against cold ischemia reperfusion injury. METHODS: Steatotic livers were preserved for 24 h in IGL-1  solution supplemented with or without IGF-1 and then perfused "ex vivo " for 2 h at 37℃. We examined the effects of IGF-1 on hepatic damage and function (transaminases, percentage of sulfobromophthalein clearance in bile and vascular resistance). We also studied other factors associated with the poor tolerance of fatty livers to cold ischemia reperfusion injury such as mitochondrial damage, oxidative stress, nitric oxide, tumor necrosis factor-α (TNF-α) and mitogen-activated protein kinases.RESULTS: Steatotic livers preserved in IGL-1 solutionsupplemented with IGF-1 showed lower transaminase levels, increased bile clearance and a reduction in vascular resistance when compared to those preserved in IGL-1solution alone. These benefits are mediated by activation of AKT and constitutive endothelial nitric oxide synthase (eNOS), as well as the inhibition of inflammatory cytokines such as TNF-α. Mitochondrial damage and oxidative stress were also prevented.CONCLUSION: IGL-1  enrichment with IGF-1 increasedfatty liver graft preservation through AKT and eNOS activation, and prevented TNF-α release during normothermic reperfusion.
引用
收藏
页码:5693 / 5700
页数:8
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