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      Bioactive Compounds from Germinated Brown Rice Protect Cardiomyocytes Against Simulated Ischemic/Reperfusion Injury by Ameliorating Mitochondrial Dysfunction

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          Abstract

          Purpose

          Ischemic/reperfusion (I/R) injury is the principal mechanism during Ischemic Heart Disease (IHD). The key modulator of I/R injury is dysregulation of mitochondria function. Germinated Brown Rice (GBR) has been recommended as a bio-functional food and has clarified the potential properties in several effects. However, the effect of GBR mediated cardioprotective properties, focusing on mitochondrial function’s role, remains unexplored. Thus, this study aims to investigate the cardioprotective effects of GBR pretreatment against simulated I/R injury.

          Methods

          H9c2 cardiomyocytes were incubated with GBR at a five ƞg/mL concentration for 24 hours and simulated I/R (sI/R) for 40 minutes. Cell viability and cell apoptosis were assessed by 7-AAD staining and Annexin V/PI staining, respectively. The mitochondrial membrane potential was determined by JC-1 staining and mitochondrial respiration represented by oxygen consumption rate (OCR) using Seahorse Flux analyzer.

          Results

          The results revealed that the administration of GBR before sI/R significantly decreased the percentage of cell death and total cell apoptosis in H9c2 during stimulation of ischemic/reperfusion. Besides, pretreatment of cardiomyocytes with GBR remarkably stabilized mitochondrial membrane potential and improved impaired mitochondrial respiration in simulated-H9c2 injury.

          Conclusion

          The present research is the first study to report the effective cardioprotection of GBR. Pretreatment of GBR potentially protects H9c2 cardiomyocytes against sI/R injury through mitochondrial function. The underlying therapeutic activities are possibly associated with its bio-functional compounds. However, the underlying mechanism on the cardioprotective effects of GBR needs further studies.

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          Most cited references 50

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          Heart Disease and Stroke Statistics—2019 Update: A Report From the American Heart Association

          Circulation, 139(10)
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            Current Mechanistic Concepts in Ischemia and Reperfusion Injury.

            Ischemia-reperfusion injury is associated with serious clinical manifestations, including myocardial hibernation, acute heart failure, cerebral dysfunction, gastrointestinal dysfunction, systemic inflammatory response syndrome, and multiple organ dysfunction syndrome. Ischemia-reperfusion injury is a critical medical condition that poses an important therapeutic challenge for physicians. In this review article, we present recent advances focusing on the basic pathophysiology of ischemia-reperfusion injury, especially the involvement of reactive oxygen species and cell death pathways. The involvement of the NADPH oxidase system, nitric oxide synthase system, and xanthine oxidase system are also described. When the blood supply is re-established after prolonged ischemia, local inflammation and ROS production increase, leading to secondary injury. Cell damage induced by prolonged ischemia-reperfusion injury may lead to apoptosis, autophagy, necrosis, and necroptosis. We highlight the latest mechanistic insights into reperfusion-injury-induced cell death via these different processes. The interlinked signaling pathways of cell death could offer new targets for therapeutic approaches. Treatment approaches for ischemia-reperfusion injury are also reviewed. We believe that understanding the pathophysiology ischemia-reperfusion injury will enable the development of novel treatment interventions.
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              Myocardial ischemia-reperfusion injury: a neglected therapeutic target.

              Acute myocardial infarction (MI) is a major cause of death and disability worldwide. In patients with MI, the treatment of choice for reducing acute myocardial ischemic injury and limiting MI size is timely and effective myocardial reperfusion using either thombolytic therapy or primary percutaneous coronary intervention (PPCI). However, the process of reperfusion can itself induce cardiomyocyte death, known as myocardial reperfusion injury, for which there is still no effective therapy. A number of new therapeutic strategies currently under investigation for preventing myocardial reperfusion injury have the potential to improve clinical outcomes in patients with acute MI treated with PPCI.
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                Author and article information

                Journal
                Drug Des Devel Ther
                Drug Des Devel Ther
                dddt
                dddt
                Drug Design, Development and Therapy
                Dove
                1177-8881
                09 March 2021
                2021
                : 15
                : 1055-1066
                Affiliations
                [1 ]Graduate School, Program of Bio-Veterinary Science, Kasetsart University , Kamphaeng Saen, Nakorn Pathom, Thailand
                [2 ]Department of Biochemistry, Faculty of Medicine Siriraj Hospital, Mahidol University , Bangkok, Thailand
                [3 ]Department of Large Animal and Wildlife Clinical Sciences, Faculty of Veterinary Medicine, Kasetsart University, Kamphaeng Saen Campus , Nakorn Pathom, Thailand
                Author notes
                Correspondence: Soontaree Petchdee Department of Large Animal and Wildlife Clinical Sciences, Faculty of Veterinary Medicine, Kasetsart University , Kamphaeng Saen, Nakorn Pathom, 73140, ThailandTel +66 34 351901-3Fax +66 34 351405 Email fvetstr@ku.ac.th
                Article
                294779
                10.2147/DDDT.S294779
                7955705
                © 2021 Demeekul 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. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Figures: 4, Tables: 2, References: 50, Pages: 12
                Funding
                Funded by: the National Research Council of Thailand for The Royal Golden Jubilee Ph.D. Program to KD;
                This research was funded by the National Research Council of Thailand for The Royal Golden Jubilee Ph.D. Program to KD [grant no. PHD/0142/2561].
                Categories
                Original Research

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