Amelioration of hepatic ischemia/reperfusion injury with intercellular adhesion molecule-1 antisense oligodeoxynucleotides.
Dumont-UCLA Liver Transplant Center, Los Angeles, CA, USA.Transplantation Proceedings (Impact Factor: 0.95). 02/2001; 33(1-2):538. DOI: 10.1016/S0041-1345(00)02130-8
- Transplantation Proceedings 01/2011; 43(1):3-29. · 0.95 Impact Factor
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ABSTRACT: To determine if blockade of P-selectin in the isolated blood-perfused cold ex vivo rat liver model protects the liver from ischemia-reperfusion injury. The effect of P-selectin blockade was assessed by employing an isolated blood-perfused cold ex vivo rat liver with or without P-selectin antibody treatment before and after 6 h of cold storage in University of Wisconsin solution. In our isolated blood-perfused rat liver model, pre-treatment with P-selectin antibody failed to protect the liver from ischemia-reperfusion injury, as judged by the elevated aspartate aminotransferase activity. In addition, P-selectin antibody treatment did not significantly reduced hepatic polymorphonuclear leukocyte accumulation after 120 min of perfusion. Histological evaluation of liver sections obtained at 120 min of perfusion showed significant oncotic necrosis in liver sections of both ischemic control and P-selectin antibody-treated groups. However, total bile production after 120 min of perfusion was significantly greater in P-selectin antibody-treated livers, compared to control livers. No significant difference in P-selectin and ICAM-1 mRNAs and proteins, GSH, GSSG, and nuclear NF-kappaB was found between control and P-selectin antibody-treated livers. In conclusion, we have shown that blockade of P-selectin alone failed to reduced polymorphonuclear leukocyte accumulation in the liver and protect hepatocytes from ischemia-reperfusion injury in the isolated blood-perfused cold-ex vivo rat liver model.World Journal of Gastroenterology 12/2008; 14(44):6808-16. · 2.55 Impact Factor
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ABSTRACT: As the natural resistance-associated macrophage protein 1 Nramp1 (also known as Slc11a1) modulates Kupffer cell (KC) activation, and KC are responsible for the early phase of warm ischemia/reperfusion (I/R) to the liver, we hypothesized that livers of Nramp1(-/-) mice will be protected from early-phase I/R injury compared with livers of Nramp1(+/+) mice. To test our hypothesis, we induced partial warm ischemia to the livers of Nramp1(+/+) and Nramp1(-/-) mice for 45 min of by clamping the hilum of the median and left lateral lobes, followed by 30 or 60 min of reperfusion. Plasma glutamate oxaloacetate transaminase (pGOT) activity and tumor necrosis factor alpha (TNF-alpha) levels were measured, and liver sections were stained for polymorphonuclear leukocyte (PMN) accumulation. After 45 min of ischemia and 30/60 min of reperfusion of Nramp1(+/+) and Nramp1(-/-) mice livers, we found significant increases in plasma pGOT activity and TNF-alpha levels in Nramp1(+/+) mice at 30 and 60 min of reperfusion, respectively, compared with sham controls and all Nramp1(-/-) mice. A significant accumulation of PMNs was also found in livers of Nramp1(+/+) mice at 60 min of reperfusion compared with all other groups. We have shown that disruption of the Nramp1 gene attenuates I/R injury to the mouse liver during the early phase of warm I/R injury. An increased understanding of the role played by Nramp1 is particularly important in the liver, as this organ is subjected to a wide variety of injuries during hemorrhagic shock, partial resections, and transplantation.Journal of Leukocyte Biology 12/2002; 72(5):885-97. · 4.57 Impact Factor
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