Preconditioning donor liver withNodosinperfusion lessens rat ischemia reperfusion injury via heme oxygenase‐1 upregulation

Aspartate transaminase Ischemic Preconditioning Ex vivo Zinc protoporphyrin
DOI: 10.1111/j.1440-1746.2011.06966.x Publication Date: 2011-11-18T18:52:22Z
ABSTRACT
Ischemia reperfusion injury (IRI) remains a major cause of graft injury, dysfunction and even failure post-transplantation. Heme oxygenase 1 (HO-1) has been found to be an attractive target for anti-inflammatory therapies potential candidate responsible cell injury. The objective this study was investigate whether preconditioning the donor liver with Nodosin perfusion upregulates HO-1 then lessens IRI in rat models.Wistar rats were divided into four groups: experimental group, control positive group negative which preconditioned Nodosin, lactated ringer's solution, cobalt protoporphyrin zinc perfusion, respectively. We measured expression enzyme activity livers each ex vivo at 0, 2 h after perfusion. At Wistar transplanted Sprague-Dawley orthotopically. Serum transaminase levels, degree apoptosis Suzuki's score used assess ischemia/reperfusion recipients 24 transplantation.Ex vivo, induced significantly, compared (P < 0.05). In serum representative lower than that Preconditioning protein mainly Kupffer cells.This suggests provides protective effect through inducing attenuate transplantation.
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