Jia R P, Xie J J, Luo F Y, Zhu J G
Department of Urology and Renal Transplantation, Nanjing First Hospital Affiliated to Nanjing Medical University, Nanjing, Pepole's Republic of China.
Transplant Proc. 2008 Dec;40(10):3316-20. doi: 10.1016/j.transproceed.2008.06.113.
The aim of this study was to investigate the early protection of ischemic preconditioning (IPC) and its mechanisms in transplanted rat kidneys.
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-alpha), IkappaB kinase-beta (IKK-beta), and nuclear factor-kappa B (NF-kappaB) P65 subunit mRNA expressions.
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-alpha 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-beta mRNA and P65 mRNA expressions between groups C and B (P > .05).
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-alpha and on positive feedback signaling of TNF-alpha/NF-kappaB pathways may play important roles in renal graft protection in the early stage.
本研究旨在探讨缺血预处理（IPC）对大鼠移植肾的早期保护作用及其机制。
36只雄性Sprague-Dawley（SD）大鼠供体和受体被随机分为以下几组：假手术组（A组；n = 6）；未处理移植组（B组；n = 6）；处理组（C组；n = 6）。A组进行剖腹探查术。B组接受原位移植。C组在原位移植前经历15分钟的缺血期，随后再灌注10分钟。我们评估血清肌酐（SCr）、血尿素氮（BUN），并评估肾移植缺血/再灌注损伤的程度：肿瘤坏死因子-α（TNF-α）、IκB激酶-β（IKK-β）和核因子-κB（NF-κB）P65亚基mRNA表达。
C组和B组的SCr和BUN水平高于假手术组（P <.01），但移植后24小时C组和B组之间无显著差异（P >.05）。与B组相比，C组肾移植肾小管损伤程度明显较轻（P <.01）。移植后24小时TNF-α转录水平明显低于非IPC组（P <.01）。然而，C组和B组之间IKK-β mRNA和P65 mRNA表达无显著差异（P >.05）。
1个周期的预处理方案（15分钟/10分钟）减轻了早期肾移植缺血/再灌注损伤。IPC可改善缺血/再灌注损伤后大鼠同种异体肾移植功能。对TNF-α以及TNF-α/NF-κB途径正反馈信号的抑制作用可能在早期肾移植保护中起重要作用。
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