The effect of NF-κB and correlated inflammatory factors in rat donor liver after cold preservation / 西安交通大学学报(医学版)

ABSTRACT

Objective To establish a model of rat orthotopic liver transplantation and investigate the relationship among cold preservation time, activation of nuclear transcription factor-κB (NF-κB) and donor preservation injury after liver transplantation. Methods Orthotopic liver transplantation was performed in Wistar rats which were randomly divided into the following groups according to the different duration of liver cold storage in UW solution group A (sham operation, n=10), group B NF-κB in liver before and after transplantation was measured by electrophoretic mobility shift assays; protein expression of tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) in the liver was measured by immunohistochemistry; the serum TNFα and IL-1β, alanine aminotransferase (ALT), aspartate aminotransferase (AST) and hepatic cell apoptosis were examined. Results With extended cold storage duration, the activity of NF-κB in the donor liver increased (P<0.05, group D vs. groups A, B and C). TNF-α and IL-1β levels also increased (P<0.05, group D vs. groups A, B and C). Donor liver reperfusion injury was gradually aggravated with the prolonging of graft cold preservation. Both the serum TNF-α and IL-1β levels increased highly (P<0.05 group A vs. groups B, C and D),NF-κB in the liver significantly increased (P<0.05, group A vs. groups D, B and C) with gradual prolonging of graft cold preservation time. The serum ALT and AST level and apoptosis index level elevated greatly (P<0.05, group A vs. groups D, B and C). Conclusion NF-κB of donor liver was activated inductively in cold preservation phase and activated explosively in reperfusion phase. The longer cold preservation time was, the higher NF-κB level in donor liver became. NF-κB led to the expression of TNF-α and IL-1β in donor liver. Inflammatory factors are one of the most important mechanisms for the donor liver injury after liver transplantation.