ISSN 2415-3060 (print), ISSN 2522-4972 (online)
  • 6 of 59
JMBS 2020, 5(5): 53–59
Experimental Medicine and Morphology

Dynamics of Mitochondrial Transmembrane Potential Changes in Blood Monocytes in Conditions of Development and Course of Experimental Periodontitis and the Effect of Korvityn on it

Demkovych A. Ye., Machogan V. R.

Inflammatory diseases of periodontal tissues remain one of the most complex and unresolved problems of modern dentistry. The most important internal stimulus for triggering apoptosis is DNA damage in response to various factors (including reactive oxygen species). Mitochondrial transmembrane potential (Δψm) is generated by the electrochemical gradient of protons on both sides of the membrane and is closely related to the functioning of mitochondria, its support is provided by the processes of electron transfer in the respiratory chain. The purpose of our study was to elucidate the pathogenetic role of changes in mitochondrial transmebranic potential in the dynamics of the inflammatory response in experimental bacterial-immune periodontitis and the effects of quercetin (Korvityn) on it. Material and methods. The study was performed on white clinically healthy rats. Experimental bacterial-immune periodontitis in experimental animals was induced by injection of a mixture of microorganisms diluted with egg protein into the tissues of the periodontal complex. Quercetin was administered by intramuscular injection for correction. Evaluation of changes in mitochondrial transmembrane potential of leukocytes was performed by flow cytofluorimetry. Results and discussion. In experimental bacterial-immune periodontitis, the percentage of cells with reduced mitochondrial transmembrane potential among blood monocytes significantly increased. In animals on the 7th day of the study, the number of cells with reduced mitochondrial transmembrane potential among blood monocytes increased significantly compared with the control group. For the next study period (14th day), the number of cells with reduced ∆ψm decreased compared to the 7th day of the experiment. Having analyzed the data of mitochondrial transmembrane potential of blood monocytes on the 30th day of the experiment, we noted that they decreased relative to those obtained on the 14th day of the study, indicating profound oxidative imbalance in cells and destabilization of the mitochondrial membrane. The use of quercetin led to a decrease in the values compared to the data of animals with our simulated pathology on the 14th day, the experiment without the introduction of flavonol, but they remained significantly higher than the control group of animals. Conclusion. Flavonol (Korvityn) quercetin reduced mitochondrial transmembrane potential in experimental bacterial-immune periodontitis, which was evidence by stabilization and attenuation of the inflammatory process

Keywords: periodontitis, monocyte, mitochondrial transmembrane potential, inflammation, flavonol

Full text: PDF (Rus) 376K

  1. Boyer E, Martin B, Le Gall‐David S, Fong S, Deugnier Y, Bonnaure‐Mallet M, et al. Periodontal pathogens and clinical parameters in chronic periodontitis. Molecular Oral Microbiology. 2019; 35(1): 19-28.
  2. Mann J, Bernstein Y, Findler M. Periodontal disease and its prevention, by traditional and new avenues (Review). Experimental And Therapeutic Medicine. 2019; 19(2): 1504-6.
  3. Bäumer A, Weber D, Staufer S, Pretzl B, Körner G, Wang Y. Tooth loss in aggressive periodontitis: Results 25 years after active periodontal therapy in a private practice. Journal Of Clinical Periodontology. 2019; 47(2): 223-32.
  4. Demkovych A, Bondarenko Yu, Hasiuk P. Effects of quercetin on antioxidant potential in the experimental periodontitis development. Interventional Medicine and Applied Science. 2019; 11(1): 60-4.
  5. Gleichmann M, Mattson MP. Neuronal Calcium Homeostasis and Dysregulation. Antioxidants & Redox Signaling. 2011; 14(7): 1261-73.
  6. Hauck AK, Bernlohr DA. Oxidative stress and lipotoxicity. Journal of Lipid Research. 2016; 57(11): 1976-86.
  7. Orrenius S, Gogvadze V, Zhivotovsky B. Calcium and mitochondria in the regulation of cell death. Biochemical and Biophysical Research Communications. 2015; 460(1): 72-81.
  8. Herrmann JM, Meyle J. Neutrophil activation and periodontal tissue injury. Periodontol. 2000. 2015; 69(1): 111-27.
  9. Rovere La RML, Roest G, Bultynck G, Parys JB. Intracellular Ca2+ signaling and Ca2+ microdomains in the control of cell survival, apoptosis and autophagy. Cell Calcium. 2016; 60(2): 74-87.
  10. Peruzzo R, Costa R, Bachmann M, Leanza L, Szabò I. Mitochondrial Metabolism, Contact Sites and Cellular Calcium Signaling: Implications for Tumorigenesis. Cancers (Basel). 2020; 12(9): 2574.
  11. Ray P, Huang B, Tsuji Y. Reactive oxygen species (ROS) homeostasis and redox regulation in cellular signaling. Cell Signal. 2012; 24(5): 981-90.
  12. Carullo G, Cappello AR, Frattaruolo L, Badolato M, Armentano B, Aiello F. Quercetin and derivatives: useful tools in inflammation and pain management. Future Med. Chem. 2017; 9(1): 79-93.
  13. Massi A, Bortolini O, Ragno D, Bernardi T, Sacchetti G, Tacchini M, et al. Research Progress in the Modification of Quercetin Leading to Anticancer Agents. Molecules. 2017; 22(8): 1270.
  14. Demkovych A. Effects of flavonol quercetin on activity of lipid peroxide oxidation in experimental bacterial-immune periodontitis. Interventional Medicine and Applied Science. 2019; 11(1): 55-9.
  15. Demkovych AYe, Bondarenko YuI. Patohenetychni osnovy modelyuvannya parodontytu u tvaryn [Pathogenetic basis periodontitis modeling in rats]. Zdobutky klinichnoi i eksperymentalnoi medytsyny – Achiev of Clin and Exper Med. 2015; 1(22): 54-7. [Ukrainian]
  16. Fossati G, Moulding D, Spiller D, Moots R, White M, Edwards S. The Mitochondrial Network of Human Neutrophils: Role in Chemotaxis, Phagocytosis, Respiratory Burst Activation, and Commitment to Apoptosis. The Journal of Immunology. 2003; 170(4): 1964-72.
  17. Berger RL, Casella C. Hypothesis Testing in Statistics. International Encyclopedia of the Social & Behavioral Sciences. 2015; 11: 491-3.
  18. Cheraghi G, Hajiabedi E, Niaghi B, Nazari F, Naserzadeh P, Hosseini MJ. High doses of sodium tungstate can promote mitochondrial dysfunction and oxidative stress in isolated mitochondria. J Biochem Mol Toxicol. 2019; 33(4): e22266.
  19. Zhang T, Liu CF, Zhang TN, Wen R, Song WL. Overexpression of Peroxisome Proliferator-Activated Receptor γ Coactivator 1-α Protects Cardiomyocytes from Lipopolysaccharide-Induced Mitochondrial Damage and Apoptosis. Inflammation. 2020; 43(5): 1806-1820.
  20. Gordan R, Fefelova N, Gwathmey JK, Xie LH. Iron Overload, Oxidative Stress and Calcium Mishandling in Cardiomyocytes: Role of the Mitochondrial Permeability Transition Pore. Antioxidants (Basel). 2020; 9(8): 758.
  21. Terao J. Factors modulating bioavailability of quercetin-related flavonoids and the consequences of their vascular function. Biochem Pharmacol. 2017; 139: 15-23.