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Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: https://hdl.handle.net/2445/189205
Hypoxia inducible factor-1α accumulation in steatotic liver preservation: role of nitric oxide
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AIM: To examine the relevance of hypoxia inducible factor (HIF-1) and nitric oxide (NO) on the preservation of fatty liver against cold ischemia-reperfusion injury (IRI). METHODS: We used an isolated perfused rat liver model and we evaluated HIF-1α in steatotic and non-steatotic livers preserved for 24 h at 4°C in University of Wisconsin and IGL-1 solutions, and then subjected to 2 h of normothermic reperfusion. After normoxic reperfusion, liver enzymes, bile production, bromosulfophthalein clearance, as well as HIF-1α and NO [endothelial NO synthase (eNOS) activity and nitrites/nitrates] were also measured. Other factors associated with the higher susceptibility of steatotic livers to IRI, such as mitochondrial damage and vascular resistance were evaluated. RESULTS: A significant increase in HIF-1α was found in steatotic and non-steatotic livers preserved in IGL-1 after cold storage. Livers preserved in IGL-1 showed a significant attenuation of liver injury and improvement in liver function parameters. These benefits were enhanced by the addition of trimetazidine (an anti-ischemic drug), which induces NO and eNOS activation, to IGL-1 solution. In normoxic reperfusion, the presence of NO favors HIF-1α accumulation, promoting also the activation of other cytoprotective genes, such as heme-oxygenase-1. CONCLUSION: We found evidence for the role of the HIF-1α/NO system in fatty liver preservation, especially when IGL-1 solution is used.
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ZAOUALI, Mohamed amine, BEN MOSBAH, Ismail, BONCOMPAGNI, Eleonora, BEN ABDENNEBI, Hassen, MITJAVILA CORS, Maria teresa, BARTRONS BACH, Ramon, FREITAS, Isabel, RIMOLA CASTELLÁ, Antonio, ROSELLÓ CATAFAU, Juan. Hypoxia inducible factor-1α accumulation in steatotic liver preservation: role of nitric oxide. _World Journal of Gastroenterology_. 2010. Vol. 16, núm. 28, pàgs. 3499-3509. [consulta: 20 de gener de 2026]. ISSN: 1007-9327. [Disponible a: https://hdl.handle.net/2445/189205]