Abstract | AIM: METHODS: RESULTS: Steatotic livers preserved in IGL-1 solution supplemented 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 increased fatty liver graft preservation through AKT and eNOS activation, and prevented TNF-α release during normothermic reperfusion.
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Authors | Mohamed Amine Zaouali, Susagna Padrissa-Altés, Ismail Ben Mosbah, Hassen Ben Abdennebi, Olivier Boillot, Antoni Rimola, Dalila Saidane-Mosbahi, Joan Roselló-Catafau |
Journal | World journal of gastroenterology
(World J Gastroenterol)
Vol. 16
Issue 45
Pg. 5693-700
(Dec 07 2010)
ISSN: 2219-2840 [Electronic] United States |
PMID | 21128318
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- IGL-1 solution
- Organ Preservation Solutions
- Tumor Necrosis Factor-alpha
- Nitric Oxide
- Insulin-Like Growth Factor I
- Nitric Oxide Synthase Type III
- Nos3 protein, rat
- Aspartate Aminotransferases
- Alanine Transaminase
- Proto-Oncogene Proteins c-akt
- Extracellular Signal-Regulated MAP Kinases
- p38 Mitogen-Activated Protein Kinases
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Topics |
- Alanine Transaminase
(metabolism)
- Animals
- Aspartate Aminotransferases
(metabolism)
- Bile
(metabolism)
- Cold Ischemia
(adverse effects)
- Extracellular Signal-Regulated MAP Kinases
(metabolism)
- Fatty Liver
(metabolism, pathology, surgery)
- Insulin-Like Growth Factor I
(pharmacology)
- Liver
(blood supply, drug effects, metabolism, pathology, surgery)
- Mitochondria, Liver
(drug effects, metabolism)
- Nitric Oxide
(metabolism)
- Nitric Oxide Synthase Type III
(metabolism)
- Organ Preservation Solutions
(pharmacology)
- Oxidative Stress
(drug effects)
- Proto-Oncogene Proteins c-akt
(metabolism)
- Rats
- Rats, Zucker
- Reperfusion Injury
(etiology, metabolism, pathology, prevention & control)
- Time Factors
- Tumor Necrosis Factor-alpha
(metabolism)
- Vascular Resistance
- p38 Mitogen-Activated Protein Kinases
(metabolism)
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