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      Effect of picroside II on hind limb ischemia reperfusion injury in rats

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          Abstract

          Introduction

          Many structural and functional damages are observed in cells and tissues after reperfusion of previously viable ischemic tissues. Acute ischemia reperfusion (I/R) injury of lower extremities occurs especially when a temporary cross-clamp is applied to the abdominal aorta during aortic surgery. Research regarding the treatment of I/R injury has been increasing day-by-day. In this study, we aimed to investigate the effect of picroside II on skeletal muscle of rats experiencing simulated I/R.

          Materials and methods

          Twenty-four male Wistar albino rats weighing between 210 and 300 g were used in this study. Rats were randomly divided into 4 groups of 6 rats each (control, I/R, control + picroside II, and I/R + picroside II). The infrarenal section of the abdominal aorta was occluded with an atraumatic microvascular clamp in I/R group. The clamp was removed after 120 minutes and reperfusion was provided for a further 120 minutes. Picroside II (10 mg kg −1) was administered intraperitoneally to the animals in control + picroside II and I/R + picroside II groups. At the end of the study, skeletal muscle tissue was obtained for the determination of total oxidant status (TOS) and total antioxidant status (TAS) levels. Apoptosis was evaluated by TUNEL experiment.

          Results

          TOS levels were significantly higher in I/R group than that of control and I/R + picroside II groups ( P=0.014, P=0.005, respectively). TAS levels were significantly higher in I/R group than that of control and I/R + picroside II groups ( P=0.007 P=0.005, respectively). TUNEL assay revealed that picroside II reduced cell necrosis.

          Conclusion

          The results of this study demonstrated that picroside II plays a critical role to prevent I/R injury. Even though our results were found to be satisfactory, it should be encouraging to those who want to conduct future research on this topic.

          Most cited references30

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          Free Radicals in Biology and Medicine

          "This latest edition has been comprehensively rewritten and updated (over 80% of the text is new), whilst maintaining the clarity of its predecessor. There is expanded coverage of isoprostanes and related compounds, mechanisms of oxidative damage to DNA and proteins (and the repair of such damage), the free radical theory of ageing and the roles played by reactive species in signal transduction, cell death, human reproduction, and other important biological events. Greater emphasis has also been placed on the methods available to measure reactive species and oxidative damage (and their potential pitfalls), as well as the importance of antioxidants in the human diet." "This book is recommended as a comprehensive introduction to the field for students, clinicians and researchers, and an invaluable companion to all those interested in the role of free radicals in the life and medical sciences."--BOOK JACKET.
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            Pathogenesis of myocardial ischemia-reperfusion injury and rationale for therapy.

            Since the initial description of the phenomenon by Jennings et al 50 years ago, our understanding of the underlying mechanisms of reperfusion injury has grown significantly. Its pathogenesis reflects the confluence of multiple pathways, including ion channels, reactive oxygen species, inflammation, and endothelial dysfunction. The purposes of this review are to examine the current state of understanding of ischemia-reperfusion injury, as well as to highlight recent interventions aimed at this heretofore elusive target. In conclusion, despite its complexity our ongoing efforts to mitigate this form of injury should not be deterred, because nearly 2 million patients annually undergo either spontaneous (in the form of acute myocardial infarction) or iatrogenic (in the context of cardioplegic arrest) ischemia-reperfusion. Copyright (c) 2010 Elsevier Inc. All rights reserved.
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              Reactive oxygen species, cell signaling, and cell injury.

              Oxidative stress has traditionally been viewed as a stochastic process of cell damage resulting from aerobic metabolism, and antioxidants have been viewed simply as free radical scavengers. Only recently has it been recognized that reactive oxygen species (ROS) are widely used as second messengers to propagate proinflammatory or growth-stimulatory signals. With this knowledge has come the corollary realization that oxidative stress and chronic inflammation are related, perhaps inseparable phenomena. New pharmacological strategies aimed at supplementing antioxidant defense systems while antagonizing redox-sensitive signal transduction may allow improved clinical management of chronic inflammatory or degenerative conditions, including Alzheimer's disease. Introduction of antioxidant therapies into mainstream medicine is possible and promising, but will require significant advances in basic cell biology, pharmacology, and clinical bioanalysis.
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                Author and article information

                Journal
                Drug Des Devel Ther
                Drug Des Devel Ther
                Drug Design, Development and Therapy
                Drug Design, Development and Therapy
                Dove Medical Press
                1177-8881
                2017
                26 June 2017
                : 11
                : 1917-1925
                Affiliations
                [1 ]Department of Cardiovascular Surgery, Gazi University Medical Faculty, Ankara
                [2 ]Department of Cardiovascular Surgery, Kahramanmaras Sutcu Imam Medical Faculty, Kahramanmaras
                [3 ]Department of Cardiovascular Surgery, Ardahan State Hospital, Ardahan
                [4 ]Department of Physiology, Ankara University Medical Faculty
                [5 ]Department of Histology and Embryology, Ankara University Medical Faculty
                [6 ]Department of Anaesthesiology and Reanimation, Gazi University Medical Faculty, Ankara
                [7 ]Department of Physiology, Dumlupinar University Medical Faculty, Kütahya, Turkey
                Author notes
                Correspondence: Mustafa Arslan, Department of Anesthesiology and Reanimation, Gazi University Medical Faculty, 06510 Ankara, Turkey, Tel +90 312 202 67 39, Email marslan36@ 123456yahoo.com
                Article
                dddt-11-1917
                10.2147/DDDT.S132401
                5500556
                5d91b146-b65c-422f-bfe3-9a4400c434aa
                © 2017 Kılıç et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

                History
                Categories
                Original Research

                Pharmacology & Pharmaceutical medicine
                ischemia reperfusion,picroside ii,hind limb skeletal muscle,tos,tas

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