抗氧化和抗炎纳米颗粒对肾缺血再灌注损伤的保护作用

S. Banaei
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引用次数: 0

摘要

背景与目的:终末期肾病(ESRD)患者在肾移植过程中发生肾缺血再灌注(IR)损伤,从而激活免疫反应。细胞因子水平升高引起的炎症反应可导致急性肾损伤(AKI),导致肾移植物损失和移植物功能障碍。本研究的目的是综述纳米颗粒对AKI的治疗作用。方法:从2000年到2020年,使用Scopus、PubMed和Google Scholar数据库,对AKI模型的相关研究确定了一种全面的搜索策略。搜索策略包括缺血再灌注和纳米颗粒等关键词。结果:再灌注期产生氧自由基,引起脂质过氧化,促进组织损伤。DNA和蛋白质的氧化损伤以及脂质膜过氧化可导致细胞死亡和凋亡。减少缺血再灌注引起的组织损伤的一些策略是纳米材料。抗氧化剂纳米颗粒可以减少组织中的氧化应激。此外,它们在向缺血细胞递送治疗剂和药物以及在分子或细胞水平上对缺血区域成像方面具有灵活性。结论:抗氧化和抗炎纳米颗粒在诊断和治疗肾缺血区域方面的潜力是新疗法开发的创新,也是近年来医学进步的独特成就。
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The Protective Effect of Antioxidant and Anti-inflammatory Nanoparticles in Renal Ischemia-Reperfusion Damage
Background& objectives: Renal ischemia-reperfusion (IR) damage occurs during renal transplantation in end-stage renal disease (ESRD) patients which activate immune responses. Inflammatory responses by increased levels of cytokines can lead to acute kidney injury (AKI) that contributes to the loss of renal grafts and graft dysfunction. The purpose of this study was to review the therapeutic effects of nanoparticles in AKI. Methods: A comprehensive search strategy was identified relevant studies on AKI models, using the Scopus, PubMed and Google Scholar databases, from 2000 until 2020. The search strategy included keywords like ischemia-reperfusion and nanoparticles. Results: Oxygen free radicals are produced during the reperfusion phase, which cause lipid peroxidation and promote tissue damage. Oxidative damage to DNA and proteins and lipid membrane peroxidation can cause cell death and apoptosis. Some strategies to reduce the tissue damage caused by ischemia-reperfusion are nanoscale materials. Antioxidant nanoparticles reduce oxidative stress in tissues. Also, they have flexibility in the delivery of therapeutic agents and drugs to the ischemic cells, and imaging of the ischemic regions at the molecular or cellular level. Conclusion: This potential of antioxidant and anti-inflammatory nanoparticles in the diagnosis and treatment of renal ischemic regions is an innovation in the development of new therapies and a unique achievement in recent medical advances.
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