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1.
Transplant Proc ; 43(1): 77-9, 2011.
Article in English | MEDLINE | ID: mdl-21335159

ABSTRACT

The Institut Georges Lopez preservation solution (IGL-1) is a serum-free organ preservative that has been shown to protect steatotic livers against hepatic ischemia-reperfusion injury. Although several hypotheses have been proposed to explain the graft protection mechanisms induced by IGL-1 solution, they have not been fully investigated. This review assessed possible IGL-1 mechanisms responsible for the increased liver tolerance of ischemia-reperfusion injury with special emphasis on vasodilatator mediators such as nitric oxide, on oxidative stress prevention, on protection against mitochondrial damage, and finally on induction of cytoprotective factors.


Subject(s)
Fatty Liver/complications , Organ Preservation Solutions , Reperfusion Injury/prevention & control , Humans , Reperfusion Injury/etiology
2.
Transplant Proc ; 42(8): 3070-5, 2010 Oct.
Article in English | MEDLINE | ID: mdl-20970612

ABSTRACT

AIM: Static preservation solution is critical for liver graft outcomes, especially when steatosis is present. Institut Georges Lopez (IGL)-1 solution protects fatty livers effectively against cold ischemia reperfusion injury. Its benefits are mediated by nitric oxide and prevention of oxidative stress. The supplementation of IGL-1 with epidermal growth factor (EGF) enhances steatotic graft preservation by increasing adenosine triphosphate content, thereby mitigating oxidative stress and mitochondrial damage. METHODS: After steatotic livers were preserved for 24 hours in IGL-1 solution with or without EGF supplements, they were perfused ex vivo for 2 hours at 37°C. The benefits of EGF were assessed by evidences of hepatic damage and function--transaminases, bile production, and flow rate--as well as by other factors presumably associated with the poor tolerance of fatty livers toward cold ischemia-reperfusion injury (IRI)--energy metabolism, mitochondrial damage, oxidative stress, eNOS activity and proinflammatory interleukin (IL) beta content. RESULTS: Steatotic livers preserved in IGL-1 solutions supplemented with EGF (10 µg/L) showed lower transaminase levels, greater bile production, and ameliorated flow rates when compared to IGL-1 alone. In addition, energy metabolism deterioration, mitochondrial damage, oxidative stress, and cytokine IL-1 beta release were prevented. CONCLUSION: EGF addition to IGL-1 increased fatty liver graft preservation, thereby reducing steatotic liver damage against cold IRI.


Subject(s)
Epidermal Growth Factor/administration & dosage , Fatty Liver/pathology , Preservation, Biological , Animals , Blotting, Western , Fatty Liver/metabolism , Fatty Liver/physiopathology , Nitric Oxide Synthase Type III/metabolism , Oxidative Stress , Rats , Solutions
3.
Am J Transplant ; 10(5): 1167-77, 2010 May.
Article in English | MEDLINE | ID: mdl-20353474

ABSTRACT

We studied the contribution of matrix metalloproteinase 2 (MMP2) and matrix metalloproteinase 9 (MMP9) to the beneficial effects of preconditioning (PC) in reduced-size orthotopic liver transplantation (ROLT). We also examined the role of c-Jun N-terminal kinase (JNK) and whether it regulates MMP2 in these conditions. Animals were subjected to ROLT with or without PC and pharmacological modulation, and liver tissue samples were then analyzed. We found that MMP2, but notMMP9, is involved in the beneficial effects of PC in ROLT. MMP2 reduced hepatic injury and enhanced liver regeneration. Moreover, inhibition of MMP2 in PC reduced animal survival after transplantation. JNK inhibition in the PC group decreased hepatic injury and enhanced liver regeneration. Furthermore, JNK upregulated MMP2 in PC. In addition, we showed that Tissue inhibitors of matrix metalloproteinases 2 (TIMP2) was also upregulated in PC and that JNK modulation also altered its levels in ROLT and PC. Our results open up new possibilities for therapeutic treatments to reduce I/R injury and increase liver regeneration after ROLT, which are the main limitations in living-donor transplantation.


Subject(s)
Liver Transplantation/methods , Liver/anatomy & histology , Animals , JNK Mitogen-Activated Protein Kinases , Liver Regeneration/drug effects , Male , Matrix Metalloproteinase 2/pharmacology , Matrix Metalloproteinase 9/pharmacology , Rats , Rats, Sprague-Dawley , Tissue Inhibitor of Metalloproteinase-2/pharmacology
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