Relationship between ischemia/reperfusion injury and acute rejection of allogeneic liver transplant in rats

Transplant Proc. 2014 Jan-Feb;46(1):50-5. doi: 10.1016/j.transproceed.2013.06.019.

Abstract

Objective: This study aimed to investigate the relationship between the severity of ischemia/reperfusion (I/R) injury and the acute rejection (AR) of allogeneic liver transplants in rats.

Methods: The experimental rats were divided in different groups: normal control group (sham group, group I); syngeneic liver transplant control group (similar gene group, group II); and allogeneic liver transplant groups (groups III to VI). The rats were humanely killed at 1, 3, 5, and 7 days after transplantation or sham operation to determine the severity of I/R injury, rejection classification, and hepatocyte apoptosis. Messenger RNA (mRNA) and protein expression levels of Fas, perforin, and granzyme B were assessed in the liver tissues using real-time polymerase chain reaction and immunohistochemistry, respectively.

Results: The rejection scores of the transplanted liver tissues gradually increased until these scores were proportional to the severity of I/R injury in groups III, IV, and V. The maximum scores were reached at 7 days after transplantation as the duration of transplantation was extended. The mRNA and protein expression levels of Fas, perforin, and granzyme B were significantly increased at 1, 3, 3, 5, and 7 days after liver reperfusion in groups III, IV, and V compared with those in groups I, II, and VI (P < .05).

Conclusion: The occurrence of AR after allogeneic liver transplantation in rats was positively correlated with the severity of I/R injury. Given that I/R injury caused serious damage to the transplanted liver, the occurrence of AR consequently decreased.

MeSH terms

  • Animals
  • Apoptosis
  • Biopsy
  • Disease Models, Animal
  • Female
  • Graft Rejection*
  • Granzymes / metabolism
  • Hepatocytes / pathology
  • Humans
  • Liver / pathology
  • Liver Failure / surgery*
  • Liver Transplantation*
  • Male
  • Pore Forming Cytotoxic Proteins / metabolism
  • Rats
  • Rats, Inbred Lew
  • Rats, Sprague-Dawley
  • Reperfusion Injury / pathology*
  • fas Receptor / metabolism

Substances

  • Fas protein, rat
  • Pore Forming Cytotoxic Proteins
  • fas Receptor
  • perforin, rat
  • Granzymes
  • Gzmb protein, rat