Wang Xinning, Zhou Changcheng, Liu Jingyu, Jia Ruipeng
Department of Urology, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu 210006, China.
Center for Renal Transplantation, Nanjing First Hospital, Nanjing Medical University, Nanjing, Jiangsu 210006, China.
J Biomed Res. 2021 Jul 22;35(5):383-394. doi: 10.7555/JBR.35.20210031.
Donation after circulatory-determined death (DCD) is an important part of renal transplantation. Therefore, DCD renal transplantation animal model should be established to study the mechanism of organ injury. Here, we established a stable DCD rat renal transplantation model and investigated the dynamic regulation of graft self-repairing and antioxidant capacities with different non-heart-beating times (NHBTs). Male Sprague-Dawley rats were randomly divided into four groups with the NHBT of the donors from 0 to 15, 30, and 45 minutes. Recipients in long NHBT groups had a significantly lower survival rate and poorer graft function than those in short NHBT groups. Grafts from the 15-minute and 30-minute NHBT groups showed light and severe injury respectively at an early stage after transplantation and recovered within 7 days after transplantation, whereas the self-repairing of the grafts in the 45-minute NHBT group was delayed. The expressions of proliferating cell nuclear antigen (PCNA) and von Willebrand factor (vWF) were dependent on NHBT. The expression of antioxidant proteins paralleled graft recovery. In conclusion, the recipients can up-regulate antioxidant capacity to enhance graft self-repairing in DCD renal transplantation. Prolonged NHBT can delay the self-repairing and antioxidation of grafts.
心脏死亡后器官捐献(DCD)是肾移植的重要组成部分。因此,应建立DCD肾移植动物模型来研究器官损伤机制。在此,我们建立了稳定的DCD大鼠肾移植模型,并研究了不同非心跳时间(NHBT)下移植肾自我修复和抗氧化能力的动态调节。将雄性Sprague-Dawley大鼠随机分为四组,供体的NHBT分别为0至15、30和45分钟。长NHBT组的受体生存率显著低于短NHBT组,移植肾功能也较差。15分钟和30分钟NHBT组的移植肾在移植后早期分别表现为轻度和重度损伤,并在移植后7天内恢复,而45分钟NHBT组移植肾的自我修复延迟。增殖细胞核抗原(PCNA)和血管性血友病因子(vWF)的表达依赖于NHBT。抗氧化蛋白的表达与移植肾恢复情况平行。总之,在DCD肾移植中,受体可上调抗氧化能力以增强移植肾的自我修复。延长NHBT会延迟移植肾的自我修复和抗氧化作用。