The role of molecular chaperonins in warm ischemia and reperfusion injury in the steatotic liver: a proteomic study.

Background: The molecular basis of the increased susceptibility of steatotic livers to warm ischemia/reperfusion (I/R) injury during transplantation remains undefined. Animal model for warm I/R injury was induced in obese Zucker rats. Lean Zucker rats provided controls.

Ischemia-reperfusion injury in rat steatotic liver is dependent on NFκB P65 activation.

Background: Steatotic liver grafts tolerate ischemia-reperfusion (I/R) injury poorly, contributing to increased primary graft nonfunction following transplantation. Activation of nuclear factor kappa-B (NFκB) following I/R injury plays a crucial role in activation of pro-inflammatory responses leading to injury.

Methods: We evaluated the role of NFκB in steatotic liver injury by using an orthotopic liver transplant (OLT) model in Zucker rats (lean to lean or obese to lean) to define the mechanisms of steatotic liver injury.

Interleukin-1beta is prominent in the early pulmonary inflammatory response after hepatic injury.

Background: Acute lung injury and inflammation can occur after hepatic ischemia/reperfusion or cryoablation. The etiology of this response is uncertain although it involves NF-kappaB-mediated cytokine release from the liver.

Methods: Inflammation-specific complementary DNA microarrays were utilized to evaluate cytokine upregulation in mouse lung at 4 hours after partial-volume hepatic cryoablation with a recirculating liquid N(2) probe.