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本文引用的文献

1
Ischemic Postconditioning Alleviates Intestinal Ischemia-Reperfusion Injury by Enhancing Autophagy and Suppressing Oxidative Stress through the Akt/GSK-3/Nrf2 Pathway in Mice.缺血后处理通过激活 Akt/GSK-3/Nrf2 通路增强自噬和抑制氧化应激减轻小鼠肠缺血再灌注损伤。
Oxid Med Cell Longev. 2020 Mar 14;2020:6954764. doi: 10.1155/2020/6954764. eCollection 2020.
2
Postconditioning: "Toll-erating" mesenteric ischemia-reperfusion injury?后适应:“耐受”肠系膜缺血再灌注损伤?
Surgery. 2017 Apr;161(4):1004-1015. doi: 10.1016/j.surg.2016.09.031. Epub 2016 Nov 11.
3
Ischemic postconditioning provides protection against ischemia-reperfusion injury in intestines of rats.缺血后处理可对大鼠肠道的缺血-再灌注损伤起到保护作用。
Int J Clin Exp Pathol. 2015 Jun 1;8(6):6474-81. eCollection 2015.
4
Postconditioning attenuates acute intestinal ischemia-reperfusion injury.预处理可减轻急性肠缺血再灌注损伤。
Kaohsiung J Med Sci. 2013 Mar;29(3):119-27. doi: 10.1016/j.kjms.2012.08.021. Epub 2012 Oct 10.
5
Antioxidants in the prevention of myocardial ischemia/reperfusion injury.抗氧化剂在预防心肌缺血/再灌注损伤中的作用。
Expert Rev Clin Pharmacol. 2009 Nov;2(6):673-95. doi: 10.1586/ecp.09.41.
6
Postconditioning effect of granulocyte colony-stimulating factor is mediated through activation of risk pathway and opening of the mitochondrial KATP channels.粒细胞集落刺激因子的预处理作用是通过激活风险途径和打开线粒体 KATP 通道来介导的。
Am J Physiol Heart Circ Physiol. 2010 Oct;299(4):H1174-82. doi: 10.1152/ajpheart.00116.2010. Epub 2010 Aug 6.
7
Mitochondrial depolarization underlies delay in permeability transition by preconditioning with isoflurane: roles of ROS and Ca2+.线粒体去极化是异氟醚预处理延迟通透性转换的基础:ROS 和 Ca2+的作用。
Am J Physiol Cell Physiol. 2010 Aug;299(2):C506-15. doi: 10.1152/ajpcell.00006.2010. Epub 2010 Jun 2.
8
Limb remote ischemic preconditioning protects the spinal cord from ischemia-reperfusion injury: a newly identified nonneuronal but reactive oxygen species-dependent pathway.肢体远程缺血预处理保护脊髓免受缺血再灌注损伤:一种新发现的非神经元但依赖活性氧物质的途径。
Anesthesiology. 2010 Apr;112(4):881-91. doi: 10.1097/ALN.0b013e3181d0486d.
9
The effect of pretreatment with calcitonin gene-related peptide on attenuation of liver ischemia and reperfusion injury due to oxygen free radicals and apoptosis.降钙素基因相关肽预处理对减轻因氧自由基和细胞凋亡所致肝缺血再灌注损伤的作用。
Hepatogastroenterology. 2009 Nov-Dec;56(96):1724-9.
10
Ischemic postconditioning does not attenuate ischemia-reperfusion injury of rabbit small intestine.缺血后处理不能减轻兔小肠缺血再灌注损伤。
Vet Surg. 2010 Feb;39(2):216-23. doi: 10.1111/j.1532-950X.2009.00619.x.

活性氧作为现象机制的关键因素的联系;缺血预处理和后处理:是走向成熟还是已然成熟?

Connection of reactive oxygen species as an essential actor for the mechanism of phenomena; ischemic preconditioning and postconditioning: Come to age or ripening?

作者信息

Sengul Demet, Sengul Ilker

机构信息

Department of Pathology, Giresun University Faculty of Medicine, Giresun, Turkey.

Division of Endocrine Surgery, Giresun University Faculty of Medicine, Giresun, Turkey.

出版信息

North Clin Istanb. 2021 Dec 31;8(6):644-649. doi: 10.14744/nci.2021.78466. eCollection 2021.

DOI:10.14744/nci.2021.78466
PMID:35284791
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8848490/
Abstract

Ischemic preconditioning (IPC), in 1986, and then ischemic postconditioning (IPoC), in 2003, were determined and lots of studies on the many organs were performed about the preventive effects of these strong endogenous mechanisms on the relevant tissues against ischemia-reperfusion and their protective impressions have been emphasized by many authorities up to date. Reactive oxygen molecules are immensely active molecules, originating from molecular oxygen, playing a principal role in intracellular signalization, aging, and various pathologic conditions. Reactive oxygen species (ROS) such as superoxide anion and hydrogen peroxide are known in the pathogenesis of ischemia-reperfusion (I/R) injury. In the pathogenesis of cellular and tissue injury in I/R, the significant output of ROS in the initial phase of reperfusion, particularly between the 1 and 7 min, has been propounded as being an essential and crucial main factor for the phenomena. Even though a great deal of mechanisms has been asserted for IPC and IPoC, the distinct shielder mechanism(s) was/were not clearly proved yet. However, occupying a significant place of ROS among these forecasted mechanisms has been advocated up to date.

摘要

1986年确定了缺血预处理(IPC),2003年又确定了缺血后处理(IPoC),并且针对这些强大的内源性机制对相关组织抵御缺血再灌注的预防作用,在许多器官上开展了大量研究,迄今为止许多权威人士都强调了它们的保护作用。活性氧分子是极具活性的分子,源自分子氧,在细胞内信号传导、衰老及各种病理状况中起主要作用。超氧阴离子和过氧化氢等活性氧(ROS)在缺血再灌注(I/R)损伤的发病机制中是已知的。在I/R导致的细胞和组织损伤发病机制中,再灌注初始阶段,尤其是1至7分钟之间ROS的大量产生,被认为是这些现象的一个至关重要的主要因素。尽管已经提出了许多关于IPC和IPoC的机制,但尚未明确证明独特的保护机制。然而,迄今为止,在这些预测机制中,ROS占据重要地位的观点已得到提倡。