Ischemic Preconditioning Improves Rat Kidney Allograft Function After Ischemia/Reperfusion Injury: The Role of Tumor Necrosis Factor-Alpha

Abstract Objective The aim of this study was to investigate the early protection of ischemic preconditioning (IPC) and its mechanisms in transplanted rat kidneys. Materials and Methods Thirty-six male Sprague-Dawley (SD) rat donors and recipients were randomly divided into the following groups: sham-operated group (A; n = 6); untreated transplantation group (B; n = 6); and treatment group (C; n = 6). Group A was subjected to exploratory laparotomy. Group B received orthotopic transplantation. Group C underwent a 15-minute period of ischemia followed by a 10-minute reperfusion before orthotopic transplantation. We assessed the serum creatinine (SCr), blood urea nitrogen (BUN), and to evaluate the degree of kidney graft ischemia/reperfusion injury: tumor necrosis factor-alpha (TNF-α), IκB kinase-beta (IKK-β), and nuclear factor-kappa B (NF-κB) P65 subunit mRNA expressions. Results The levels of SCr and BUN in groups C and B were greater than in the sham-operated group ( P < .01), but there was no significant difference between the C and B groups at 24 hours after transplantation ( P > .05). The degree of renal graft tubular injury in group C was significantly less compared with group B ( P < .01). TNF-α transcription levels at 24 hours after transplantation were significantly less compared with the non-IPC group ( P < .01). However, no significant difference was observed in IKK-β mRNA and P65 mRNA expressions between groups C and B ( P > .05). Conclusions A 1-cycle schedule of preconditioning (15 min/10 min) attenuated renal graft ischemia/reperfusion injury in the early phase. IPC can improve rat kidney allograft function after ischemia/reperfusion injury. The inhibitory effects on TNF-α and on positive feedback signaling of TNF-α/NF-κB pathways may play important roles in renal graft protection in the early stage.