Українська English

ISSN 2522-9028 (Print)
ISSN 2522-9036 (Online)
DOI: https://doi.org/10.15407/fz

Fiziologichnyi Zhurnal

is a scientific journal issued by the

Bogomoletz Institute of Physiology
National Academy of Sciences of Ukraine

Editor-in-chief: V.F. Sagach

The journal was founded in 1955 as
1955 – 1977 "Fiziolohichnyi zhurnal" (ISSN 0015 – 3311)
1978 – 1993 "Fiziologicheskii zhurnal" (ISSN 0201 – 8489)
1994 – 2016 "Fiziolohichnyi zhurnal" (ISSN 0201 – 8489)
2017 – "Fiziolohichnyi zhurnal" (ISSN 2522-9028)

Fiziol. Zh. 2022; 68(4): 40-47

PECULIARITIES OF SYSTEMIC PATHOBIOCHEMICAL REACTIONS TO BRAIN ISCHEMIA-REPERFUSION IN RATS WITH DIABETES MELLITUS

О.V. Tkachuk1, S.S. Tkachuk1, М.А. Povar1, S.I. Anokhina1, O.V. Yasinska1, S.N. Vadziuk2

  1. Bukovinian State Medical University, Chernivtsi, Ukraine
  2. I.Y.Horbachevsky Ternopil National Medical University, Ternopil, Ukraine
DOI: https://doi.org/10.15407/fz68.04.040


Abstract

The objective of the research was to study the signs of oxidative stress, the state of proteolysis, and the proteinase-inhibiting system of the blood plasma in rats with streptozotocin-induced diabetes mellitus (60 mg/kg intra-abdominally), complicated by cerebral ischemia-reperfusion. Levels of products of lipid peroxide oxidation, protein oxidative modification, nitrogen oxide metabolites, and activity of the antioxidant protection enzymes were determined by means of biochemical methods one hour after completion of the reperfusion period and on the 12th day. Increased intensity of lipid peroxidation was found to occur in the blood plasma of rats without diabetes mellitus in both terms of observation. This was accompanied by an increase in the activity of all the antioxidant enzymes, while in animals with diabetes the amount of lipid peroxidation products decreased in the ground of prevailing depression of all the antioxidant protection enzymes. Irrespective of a tendency of changes in the amount of POM products with cerebral ischemia-reperfusion, their content is reliably higher in animals with diabetes mellitus in both terms of observation than those in animals without diabetes, which is indicative of a higher intensity of their oxidation. Without diabetes, the proteolytic activity of the blood plasma reacts by increasing the values of the studied parameters against the background of suppression of the proteinase inhibitory system during the entire observation period, in rats, with diabetes the parameters of plasma proteolysis and the state of the proteinase-inhibiting system remain without changes in both terms of the observation. The data obtained allowed us to state that diabetes mellitus considerably modifies the response of the systemic pathobiochemical indices to cerebral ischemia-reperfusion.

Keywords: diabetes mellitus; cerebral ischemia-reperfusion; pathobiochemical disturbances.

Full text: (PDF, in Ukrainian)

References

  1. Ozougwu JC, Obimba KC, Belonwu CD, Unakalamba CB. The pathogenesis and pathophysiology of type 1 and type 2 diabetes mellitus. J Physiol Pathophysiol. 2013;4(4):46-57. CrossRef
  2. Zaccardi F, Webb DR, Yates T, Davies MJ. Pathophysiology of type 1 and type 2 diabetes mellitus: a 90-year perspective. Postgrad Med J. 2016;92(1084):63-9. CrossRef PubMed
  3. Jebur AB, Mokhamer MH, El-Demerdash FM. A review on oxidative stress and role of antioxidants in diabetes mellitus. Austin Endocrinol Diabetes. Case Rep. 2016;1(1):1006.
  4. Sen Saikat, Chakraborty Raja, De Biplab. Oxidative Stress and Diabetes Mellitus. In: Diabetes Mellitus in 21st Century. Singapore: Springer; 2016, 55-67. CrossRef PubMedCentral
  5. Woodruff TM, Thundyil J, Tang SC, Sobey CG, Taylor SM, Arumugam TV. Pathophysiology, treatment, and animal and cellular models of human ischemic stroke. Mol Neurodegener. 2011;6(1):11. CrossRef PubMed PubMedCentral
  6. Rodrigo R, Fernández-Gajardo R, Gutiérrez R, Matamala JM, Carrasco R, Miranda-Merchak A, et al. Oxidative stress and pathophysiology of ischemic stroke: novel therapeutic opportunities. CNS Neurol Disord Drug Targets. 2013;12(5):698-714. CrossRef PubMed
  7. Kalinin RE, Abalenikhina YuV, Pshennikov AS, Suchkov IA, Isakov SA. Interrelation between oxidative carbonylation of proteins and lysosomal proteolysis of plasma in experimentally modelledischemia and ischemia-reperfusion. Eruditio Juvenium. 2017;5(3):338-51. [Russian]. CrossRef
  8. Ge P, Luo Y, Liu CL, Hu B. Protein aggregation and proteasome dysfunction after brain ischemia. Stroke. 2007;38(12):3230-6. CrossRef PubMed PubMedCentral
  9. Tkachuk OV. Effect of streptozotocin-induced diabetes and incomplite global brain ischemia on apoptosis in the rats thymus. Fiziol Zh. 2011;57(6):58-64. [Ukrainian]. CrossRef
  10. Magalyas VM, Mikheev AO, Rogovy YuE. Modern methods of experimental and clinical research of the central research laboratory of the Bukovyna State Med Acad. Chernivtsi; 2001.
  11. Green LC, Wagner DA, Glogowski J, Skipper PL, Wishnok JS, Tannenbaum SR. Analysis of nitrate, nitrite, and [15N]nitrate in biological fluids. Anal Biochem. 1982;126(1):131-8. CrossRef
  12. Veremeenko KN, Goloborodko OP, Kizim AI. Proteolysis in normal and pathological conditions. Kyiv; 1988. [Russian].
  13. Nanetti L, Taffi R, Vignini A, et al. Reactive oxygen species plasmatic levels in ischemic stroke. Mol Cell Biochem. 2007;303(1-2):19-25. CrossRef PubMed
  14. Chen H, Chen X, Luo Y, Shen J. Potential molecular targets of peroxynitrite in mediating blood-brain barrier damage and haemorrhagic transformation in acute ischaemic stroke with delayed tissue plasminogen activator treatment. Free Radic Res. 2018;52(11-12):1220-39. CrossRef PubMed
  15. Alghazeer R, Alghazir N, Awayn N, Ahtiwesh O, Elgahmasi S. Biomarkers of oxidative stress and antioxidant defense in patients with type 1 diabetes mellitus. Ibnosina J Med Biomed Sci. 2018;10:198-204. CrossRef
  16. Nagai R, Murray DB, Metz TO, Baynes JW. Chelation: a fundamental mechanism of action of AGE inhibitors, AGE breakers, and other inhibitors of diabetes complications. Diabetes. 2012;61(3):549-59. CrossRef PubMed PubMedCentral
  17. Rhee SY, Kim YS. The role of advanced glycation end products in diabetic vascular complications. Diabetes Metab J. 2018;42(3):188-95. CrossRef PubMed PubMedCentral
  18. Teodoro JS, Nunes S, Rolo AP, Reis F, Palmeira CM. Therapeutic options targeting oxidative stress, mitochondrial dysfunction and inflammation to hinder the progression of vascular complications of diabetes. Front Physiol. 2018;9:1857. CrossRef PubMed PubMedCentral
  19. Hu R, Xia CQ, Butfiloski E, Clare-Salzler M. Effect of high glucose on cytokine production by human peripheral blood immune cells and type I interferon signaling in monocytes: Implications for the role of hyperglycemia in the diabetes inflammatory process and host defense against infection. Clin Immunol. 2018;195:139-48. CrossRef PubMed PubMedCentral
  20. Queisser MA, Yao D, Geisler S, Hammes HP, Lochnit G, Schleicher ED, et al. Hyperglycemia impairs proteasome function by methylglyoxal. Diabetes. 2010;59(3):670-8. CrossRef PubMed PubMedCentral
© National Academy of Sciences of Ukraine, Bogomoletz Institute of Physiology, 2014-2024.