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心脏死亡后循环停止时间延长的肾移植捐赠修复后抗氧化的动态调节

Dynamic regulation of anti-oxidation following donation repairing after circulatory determined death renal transplantation with prolonged non-heart-beating time.

作者信息

Wang Xinning, Zhou Changcheng, Liu Jingyu, Jia Ruipeng

机构信息

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.

出版信息

J Biomed Res. 2021 Jul 22;35(5):383-394. doi: 10.7555/JBR.35.20210031.

DOI:10.7555/JBR.35.20210031
PMID:34628404
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8502692/
Abstract

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.

摘要

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。

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本文引用的文献

1
Uncontrolled Donation After Circulatory Death: A Unique Opportunity.《心跳骤停后非计划性捐献：一个独特的机会》
Transplantation. 2020 Aug;104(8):1542-1552. doi: 10.1097/TP.0000000000003139.
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Missed opportunities for DCD kidney donors: Evaluation of warm ischemic time and associated functional warm ischemic time.DCD 供肾者错失的机会：热缺血时间评估及相关功能热缺血时间。
Clin Transplant. 2019 Nov;33(11):e13724. doi: 10.1111/ctr.13724. Epub 2019 Oct 22.
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Diabetes aggravates renal ischemia and reperfusion injury in rats by exacerbating oxidative stress, inflammation, and apoptosis.
糖尿病通过加剧氧化应激、炎症和细胞凋亡加重大鼠肾缺血再灌注损伤。
Ren Fail. 2019 Nov;41(1):750-761. doi: 10.1080/0886022X.2019.1643737.
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The efficacy of HBOC-201 in ex situ gradual rewarming kidney perfusion in a rat model.HBOC-201 在大鼠模型中离体逐步复温肾脏灌注中的疗效。
Artif Organs. 2020 Jan;44(1):81-90. doi: 10.1111/aor.13534. Epub 2019 Aug 1.
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Molecular Pathways Underlying Adaptive Repair of the Injured Kidney: Novel Donation After Cardiac Death and Acute Kidney Injury Platforms.损伤肾脏的适应性修复的分子途径：新型心脏死亡后捐献和急性肾损伤平台。
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Zinc mitigates renal ischemia-reperfusion injury in rats by modulating oxidative stress, endoplasmic reticulum stress, and autophagy.锌通过调节氧化应激、内质网应激和自噬减轻大鼠肾缺血再灌注损伤。
J Cell Physiol. 2018 Nov;233(11):8677-8690. doi: 10.1002/jcp.26747. Epub 2018 May 15.
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Am J Transplant. 2018 Apr;18(4):855-867. doi: 10.1111/ajt.14567. Epub 2017 Dec 2.
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J Cell Mol Med. 2017 Dec;21(12):3381-3393. doi: 10.1111/jcmm.13249. Epub 2017 Jun 21.