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      Kidney remote ischemic preconditioning as a novel strategy to explore the accurate protective mechanisms underlying remote ischemic preconditioning


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          This study reports a novel strategy for investigating the key factors responsible for the protective effect of remote ischemic preconditioning (RIPC) against renal ischemia-reperfusion (IR) injury, which remains the leading cause of the acute kidney injury that increase the morbidity and mortality in patients with renal impairment.


          The renal blood flow of the right kidneys in kidney remote ischemic preconditioning (KRIPC) group was occluded for 20 min. After 48 h, the renal blood flow of the left kidneys of both KRIPC and IPC groups was occluded for 30 min, and mice were dissected after 7 days of the last surgery. Blood samples were analyzed by an animal blood counter. The levels of creatinine, urea nitrogen, lipid peroxidation, nitric oxide (NO), and high-density lipoproteins (HDLs) were estimated in the plasma of mice. Kidney slices were stained with 2% triphenyltetrazolium chloride (TTC) to estimate the renal infarction.


          Unlike KRIPC group, data from IPC group revealed a massive reduction in neutrophils count, a significant increase in creatinine, urea nitrogen, and HDLs levels, and an increase in the renal infarction compared with control group.


          This is the first study demonstrating KRIPC as a novel and applicable model with the goal of defining the accurate protective mechanisms underlying RIPC against IR injury.

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          Most cited references44

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          Cell biology of ischemia/reperfusion injury.

          Disorders characterized by ischemia/reperfusion (I/R), such as myocardial infarction, stroke, and peripheral vascular disease, continue to be among the most frequent causes of debilitating disease and death. Tissue injury and/or death occur as a result of the initial ischemic insult, which is determined primarily by the magnitude and duration of the interruption in the blood supply, and then subsequent damage induced by reperfusion. During prolonged ischemia, ATP levels and intracellular pH decrease as a result of anaerobic metabolism and lactate accumulation. As a consequence, ATPase-dependent ion transport mechanisms become dysfunctional, contributing to increased intracellular and mitochondrial calcium levels (calcium overload), cell swelling and rupture, and cell death by necrotic, necroptotic, apoptotic, and autophagic mechanisms. Although oxygen levels are restored upon reperfusion, a surge in the generation of reactive oxygen species occurs and proinflammatory neutrophils infiltrate ischemic tissues to exacerbate ischemic injury. The pathologic events induced by I/R orchestrate the opening of the mitochondrial permeability transition pore, which appears to represent a common end-effector of the pathologic events initiated by I/R. The aim of this treatise is to provide a comprehensive review of the mechanisms underlying the development of I/R injury, from which it should be apparent that a combination of molecular and cellular approaches targeting multiple pathologic processes to limit the extent of I/R injury must be adopted to enhance resistance to cell death and increase regenerative capacity in order to effect long-lasting repair of ischemic tissues. Copyright © 2012 Elsevier Inc. All rights reserved.
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            Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium.

            Circulation, 74(5), 1124-1136
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              Reperfusion injury and reactive oxygen species: The evolution of a concept☆

              Reperfusion injury, the paradoxical tissue response that is manifested by blood flow-deprived and oxygen-starved organs following the restoration of blood flow and tissue oxygenation, has been a focus of basic and clinical research for over 4-decades. While a variety of molecular mechanisms have been proposed to explain this phenomenon, excess production of reactive oxygen species (ROS) continues to receive much attention as a critical factor in the genesis of reperfusion injury. As a consequence, considerable effort has been devoted to identifying the dominant cellular and enzymatic sources of excess ROS production following ischemia-reperfusion (I/R). Of the potential ROS sources described to date, xanthine oxidase, NADPH oxidase (Nox), mitochondria, and uncoupled nitric oxide synthase have gained a status as the most likely contributors to reperfusion-induced oxidative stress and represent priority targets for therapeutic intervention against reperfusion-induced organ dysfunction and tissue damage. Although all four enzymatic sources are present in most tissues and are likely to play some role in reperfusion injury, priority and emphasis has been given to specific ROS sources that are enriched in certain tissues, such as xanthine oxidase in the gastrointestinal tract and mitochondria in the metabolically active heart and brain. The possibility that multiple ROS sources contribute to reperfusion injury in most tissues is supported by evidence demonstrating that redox-signaling enables ROS produced by one enzymatic source (e.g., Nox) to activate and enhance ROS production by a second source (e.g., mitochondria). This review provides a synopsis of the evidence implicating ROS in reperfusion injury, the clinical implications of this phenomenon, and summarizes current understanding of the four most frequently invoked enzymatic sources of ROS production in post-ischemic tissue.

                Author and article information

                Interv Med Appl Sci
                Interv Med Appl Sci
                Interventional Medicine & Applied Science
                Akadémiai Kiadó (Budapest )
                25 March 2017
                March 2017
                : 9
                : 1
                : 20-26
                [1 ]Zoology Department, Division of Physiology, Faculty of Science, Damanhour University , Damanhour, Egypt
                Author notes
                [* ]Corresponding address: Muobarak J. Tuorkey, PhD; Zoology Department, Division of Physiology, Faculty of Science, Damanhour University, 14 El-Gomhoria Street, Damanhour, Al-Behira 22111, Egypt; Phone: +20 198 624 037; Fax: +20 453 368 757; E-mail: physio_mj_tuorkey@ 123456yahoo.com
                © 2017 The Author(s)

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium for non-commercial purposes, provided the original author and source are credited.

                : 25 January 2017
                : 20 February 2017
                Page count
                Figures: 7, Tables: 0, Equations: 0, References: 30, Pages: 7
                Funding source: This study was performed by an institutional self support by the author.
                Original Paper

                acute kidney injury,kidney remote ischemic preconditioning,remote ischemic preconditioning,neutrophils,creatinine


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