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    Stechenko L.O., Chaikovsky Y.B., Kryvosheyeva O.I., Chuhrai S.M., Pastuhova V.A., Irkha S.V.

    FEATURES OF THE RIGHT ATRIUM STRUCTURE IN EXPERIMENTAL DIABETES MELLITUS AND USE OF ANTIOXIDANTS


    About the author: Stechenko L.O., Chaikovsky Y.B., Kryvosheyeva O.I., Chuhrai S.M., Pastuhova V.A., Irkha S.V.
    Heading EXPERIMENTAL MEDICINE
    Type of article Scentific article
    Annotation Right atrium cardiomyocytes were studied in conditions of streptozotocin-induced type 1 diabetes mellitus and with the use of N-acetylcysteine as an antioxidant. The study showed that potential damage of fine mechanisms of synthesis and secretion of atrial natriuretic peptide may be the cause of cardiovascular pathology in diabetes. Use of antioxidant drugs has revealed that N-acetylcysteine partially reduces cardiomyocyte swelling, increases the number of atrial granules containing atrial natriuretic peptide and stimulates autophagy. Based on ultrastructural studies of atrial cardiomyocytes in type 1 diabetes it was found that damage to protein synthesis and accumulation and transformation of abnormal proteins happen via their elimination in two ways: through the ubiquitin-proteasomal and autophago-lysosomal systems. Autophagosomes occur both with a double membrane, i.e. the newly formed one, and with a single membrane after contact with lysosomes. These processes take place to maintain homeostasis in cardiomyocytes and in the myocardium as a whole. Impairement of these systems may lead to development of diabetic cardiomyopathy.
    Tags type I diabetes mellitus in rats, right atrium cardiomyocytes, atrial granules, autophagy
    Bibliography
    • Buneeva OA, Medvedev AS. Ubikvitin-nezavisimaya degradatsiya belkov v proteosomakh. Biomedicinskaya khimiya 2018; 64(2):134-48. [in Russian]
    • Sitnik IM, Stechenko LO, Krivosheyeva OI, Natrus LV, Haytovich MV. Vplv N-acetiltsisteyinu ta lozartanu na modulyuvannya tsitoprotektornoyi autofahiyi v miokardi shchuriv pry eksperimentalnomu tsukrovomu diabeti 1 typu (za danymy elektronnoyi mikroskopiyi). Ukrayinskyi naukovo-medychnyi molodizhnyi zhurnal. 2017; 2(101): 25-30. [in Ukrainian]
    • Adams B, Mapanga RF, Essop MF. Partial inhibition of the ubiquitin–proteasome system ameliorates cardiac dysfunction following ischemia–reperfusion in the presence of high glucose. Cardiovasc Diabetol. 2015; 14:94–109.
    • Godar RJ, Ma X, Liu H, Murphy JT, Weinheimer CJ, Kovacs A, et al. Repetitive stimulation of autophagy-lysosome machinery by intermittent fasting preconditions the myocardium to ischemia/reperfusion injury. Autophagy. 2015; 11(9):1537–60.
    • Mei Y, Thompson MD, Cohen RA, Tong XY. Autophagy and oxidative stress in cardiovascular diseases. Biochimica et Biophysica Acta 1852. 2015; 2015: 243–51.
    • Moyzis AG, Sadoshima J, Gustafsson AB. Mending a broken heart: the role of mitophagy in cardioprotection. Am J Physiol Heart Circ Physiol. 2015; 308: H183–H192.
    • Zhang L, Ding W, Wang Zh, Tang M, Wang F., Li Y. et al. Early administration of trimetazidine attenuates diabetic cardiomyopathy in rats by alleviating fibrosis, reducing apoptosis and enhancing autophagy. J Transl Med. 2016; 14:109 -121.
    • Zhang M, Zhang L, Hu J. MST1 coordinately regulates autophagy and apoptosis in diabetic cardiomyopathy in mice. Diabetologia. 2016. doi:10.1007/s00125016-4070-9.
    • Wang S, Wang C., Yan F. N-acetylcysteine attenuates diabetic myocardial ischemia reperfusion injury through inhibiting excessive autophagy. Mediators ofInflammation.2017; ID 9257291, 10 p.
    Publication of the article «World of Medicine and Biology» №2(72), 2020 year, 208-212 pages, index UDK 616.125.3: 57.012.4:616.37-008.64:57.084.1
    DOI 10.26724/2079-8334-2020-2-72-208-212