缺血-再灌注氧化损伤机制及其对不同器官功能的影响
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1.吉林农业大学生命科学学院,长春 130118;2.吉林农业大学食药用菌教育部工程研究中心,长春 130118; 3.吉林农业大学中药材学院,长春 130118;4.人参新品种远育与开发国家地方联合工程技术研究中心,长春 130118

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R-33

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Oxidative injury mechanism of ischemia-reperfusion and its effect on various organ functions
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1. College of Life Sciences, Jilin Agricultural University, Changchun 130118, China. 2. Engineering Research Center of Edible and Medicinal Fungi, Ministry of Education, Jilin Agricultural University, Changchun 130118. 3. College of Chinese Materia Medica, Jilin Agricultural University, Changchun 130118. 4. National and Local Joint Engineering Research Center of Remote Breeding and Development of Ginseng New Varieties, Changchun 130118

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    摘要:

    缺血是由于机体组织器官梗死或者血液供应障碍等原因造成的一种局限性缺血性坏死或软化,常发生在肝、肾、脑等器官。在恢复血流供应的初期,往往会引起“缺血-再灌注损伤( ischemia reperfusion injury, IRI)”。氧化应激是诱发缺血-再灌注损伤的重要原因之一,相关研究证实缺血-再灌注氧化损伤会导致活性氧 (reactive oxygen species,ROS)产生,而 ROS 可相应引起器官损伤及功能障碍本综述主要从氧化应激角度对近些年来有关缺血-再灌注氧化损伤的研究进展进行总结,分析这种损伤对各组织器官的影响,旨在进一步揭示缺血- 再灌注氧化损伤机制,为相应疾病的预防和治疗提供思路。

    Abstract:

    Ischemia is a kind of localized ischemic necrosis or softening caused by infarction of tissues and organs or blood supply disturbance, which often occurs in the liver, kidney, brain, and other organs. In the early stage of restoring blood supply, it often causes ischemia-reperfusion injury. Oxidative stress is a major causes of ischemia- reperfusion injury. Studies have confirmed that ischemia-reperfusion leads to the production of reactive oxygen species, which causes organ injury and dysfunction. This review summarizes the research progress of ischemia-reperfusion oxidative injury in recent years from the perspective of oxidative stress and analyzes the effect of this injury on various tissues and organs. It aims to further reveal the mechanism of oxidative injury caused by ischemia-reperfusion and provide ideas for the prevention and treatment of related diseases.

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李 昕,王芷宁,付 璐,张林波,肖盛元,张文慧.缺血-再灌注氧化损伤机制及其对不同器官功能的影响[J].中国比较医学杂志,2022,32(7):149~154.

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  • 收稿日期:2021-11-12
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  • 在线发布日期: 2022-11-09
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自2024年1期开始,杂志参考文献改为中英文对照,具体格式要求可置下载中心查看!
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