Mechanism of antisurdant action of triazin-indole derivative at experimental acoustic trauma

  • Владимир Пастушенко Farm-TRISAN Ltd, 16, Serebristii bul., St. Petersburg, 197227, Russian Federation
  • Максим Кузнецов S. M. Kirov Military Medical Academy, 6, ul. Academika Lebedeva, St. Petersburg, 194044, Russian Federation
  • Владимир Дворянчиков S. M. Kirov Military Medical Academy, 6, ul. Academika Lebedeva, St. Petersburg, 194044, Russian Federation
  • Александр Пастушенко North-Western State Medical University named after I. I. Mechnikov, 41, Kirochnaya ul., St. Petersburg, 191015, Russian Federation
  • Мадина Габаева Kabardino-Balkarian State University named after H. M. Berbekov, 173, ul. Chernyshevskogo, Nalchik, Kabardino-Balkarian Republic, 360004, Russian Federation

Аннотация

In our research performed using model of acoustic trauma at experimental animals (female of hybrids F1 of CBA and C57BL/6 lines) influence of triazin-indole at expression level of hypoxia induced factor (HIF) in Corti’s organ was studied at its therapy application. As a reference drug cytoflavin was used. Investigated drug in the form of 1 % solution was introduced into animals parenterally in dosage 5, 7, 10 mg/kg with 2 hr intervals after acoustic impact. Injection of cytoflavin as reference drag was performed in 1.7 ml/kg dosage. Level of HIF expression in the drug of Corti’s organ was estimated using immunohistochemical method. It was found out that triazin-indole derivative increases HIF expression in Corti’s cells and in neurons of spiral ganglion at acoustical traumatic impact depending on drug dosage increase. Maximal HIF expression in Corti’s cells and in ganglions were noted at therapeutic dose of the drug 10 mg/kg. In control group and in the group with application citoflavin in dose 1.7 ml/kg minimal HIF expression was observed. According to obtained results of performed investigation the authors concluded that antisurdant property of triazin-indole derivative is realized through the influence on HIF metabolism (probably, by blockage of prolyl hydroxylase) and enables to consider it as a target molecular during the drug application.

Скачивания

Данные скачивания пока недоступны.
 

Литература


References

On the State of Sanitary and Epidemiological Welfare of the Population in the Russian Federation In 2019: State Report. Federal Service for Surveillance on Consumer Rights Protection and Human Wellbeing,2020, p. 134. (In Russian)

Deafness and hearing loss. Available at: https://www.who.int/ru/news-room/fact-sheets/detail/deafness- and-hearing-loss (accessed: 20.03.2019).

Adeninskaia E. E., Gorblianskii Iu. Iu., Khoruzhaia O. G. Comparative analysis of features professional employees sensorineural hearing loss in a variety of sectors. Acta Biomedica Scientifica, 2013, no. 6, pp. 87–91. (In Russian)

Ntlhakana L., Nelson G., Khoza-Shangase K. Estimating miners at risk for occupational noise-induced hearing loss: A review of data from a South African platinum mine. S. Afr. J. Commun. Disord., 2020, vol. 67, no. 2, pp. 1–8.

Yankaskas K., Hammill T., Packer M., Zuo J. Editorial: Auditory injury — A military perspective.Hear. Res., 2017, no. 349, pp. 1–3.

Muhr P., Johnson A. C., Selander J., Svensson E., Rosenhall U. Noise Exposure and Hearing Impairment in Air Force Pilots. Aerosp. Med. Hum. Perform., 2019, vol. 90, no. 9, pp. 757–763.

Petrova N. N. Modern look on ethiological and pathogenetical therapy of sensorineural hearing loss.Obzory po klinicheskoi farmakologii i lekarstvennoi terapii, 2010, no. 2, pp. 35–40. (In Russian)

Burak G. G., Samsonova I. V., Kobets Iu. G. Variants of divergence, topography and branching of labyrinthine arteries: clinical and anatomical aspects. Vestnik VGMU, 2009, vol. 8, no. 2, pp. 1–23.(In Russian)

Kurabi A., Keithley E. M., Housley G. D., Ryan A. F., Wong A. C. Cellular mechanisms of noise-induced hearing loss. Hear. Res., 2017, no. 349, pp. 129–137.

Semenza G. L., Wang G. L. A nuclear factor induced by hypoxia via de novo protein synthesis binds to the human erythropoietingene enhancer at a site required for transcriptional activation. Mol. Cell.Biol., 1992, vol. 12, no. 12, pp. 5447–5454.

Semenza G. L. Pharmacologic Targeting of Hypoxia-Inducible Factors. Annu Rev. Pharmacol. Toxicol.,2019, no. 59, pp. 379–403.

Duan C. Hypoxia-inducible factor 3 biology: complexities and emerging themes. Am. J. Physiol. Cell. Physiol., 2016, vol. 310, no. 4, pp. 260–269.

Zhang J., Zhang Q. VHL and Hypoxia Signaling: Beyond HIF in Cancer. Biomedicines, 2018, vol. 6,no. 1, p. 35.

Lanigan S. M., O’Connor J. J. Prolyl hydroxylase domain inhibitors: can multiple mechanisms be an opportunity for ischemic stroke? Neuropharmacology, 2019, no. 148, pp. 117–130.

Nagao A., Kobayashi M., Koyasu S., Chow C. C. T, Harada H. HIF-1-Dependent Reprogramming of Glucose Metabolic Pathway of Cancer Cells and Its Therapeutic Significance. Int. J. Mol. Sci., 2019, vol. 20, no. 2, p. 238.

Karagiota A., Kourti M., Simos G., Mylonis I. HIF-1α-derived cell-penetrating peptides inhibit ERKdependent activation of HIF-1 and trigger apoptosis of cancer cells under hypoxia. Cell. Mol. Life Sci., 2019, vol. 76, no. 4, pp. 809–825.

Pak J. H., Yi J., Ryu S., Kim I. K., Kim J. W., Baek H., Chung J. W. Induction of Redox-Active Gene Expression by CoCl2 Ameliorates Oxidative Stress-Mediated Injury of Murine Auditory Cells. Antioxidants(Basel), 2019, vol. 8, no. 9, p. 399.

Zhuravskii S. G. Improvement of speech discrimination with cytoflavin in patients with chronic sensorineural deafness. Vestn. Otorinolaringol., 2010, no. 4, pp. 82–86. (In Russian)

Maxwell P. H., Eckardt K. U. HIF prolyl hydroxylase inhibitors for the treatment of renal anaemia and beyond. Nat. Rev. Nephrol., 2016, vol. 12, no. 3, pp. 157–168.

HoWangYin K. Y., Loinard C., Bakker W., Guérin C. L., Vilar J., d’Audigier C., Mauge L., Bruneval P., Emmerich J., Lévy B. I., Pouysségur J., Smadja D. M., Silvestre J. S. HIF-prolyl hydroxylase 2 inhibition enhances the efficiency of mesenchymal stem cell-based therapies for the treatment of critical limbischemia. Stem. Cells, 2014, vol. 32, no. 1, pp. 231–243.

Strowitzki M. J., Cummins E. P., Taylor C. T. Protein Hydroxylation by Hypoxia-Inducible Factor (HIF) Hydroxylases: Unique or Ubiquitous? Cells, 2019, vol. 8, no. 5, p. 384.

Nagle D. G., Zhou Y. D. Natural product-derived small molecule activators of hypoxia-inducible factor-1 (HIF-1). Curr. Pharm. Des., 2006, vol. 12, no. 21, pp. 2673–2688.

Wang K., Jing Y., Xu C., Zhao J., Gong Q., Chen S. HIF-1α and VEGF Are Involved in Deferoxamine-Ameliorated Traumatic Brain Injury. J. Surg. Res., 2020, no. 246, pp. 419–426.

Wang W. S., Liang H. Y., Cai Y. J., Yang H. DMOG ameliorates IFN-γ-induced intestinal barrier dysfunction by suppressing PHD2-dependent HIF-1α degradation. J. Interferon Cytokine Res., 2014,vol. 34, no. 1, pp. 60–69.

Shafighi M., Olariu R., Fathi A. R., Djafarzadeh S., Jakob S. M., Banic A., Constantinescu M. A. Dimethyloxalylglycine stabilizes HIF-1α in cultured human endothelial cells and increases random-pattern skin flap survival in vivo. Plast. Reconstr. Surg., 2011, vol. 128, no. 2, pp. 415–422.

Mikami H., Saito Y., Okamoto N., Kakihana A., Kuga T., Nakayama Y. Requirement of Hsp105 in CoCl2-induced HIF-1α accumulation and transcriptional activation. Exp. Cell. Res., 2017, vol. 352, no. 2, pp. 225–233.

Serocki M., Bartoszewska S., Janaszak-Jasiecka A., Ochocka R. J., Collawn J. F., Bartoszewski R. miRNAs regulate the HIF switch during hypoxia: a novel therapeutic target. Angiogenesis, 2018,vol. 21, no. 2, pp. 183–202.

David B. T., Curtin J. J., Goldberg D. C., Scorpio K., Kandaswamy V., Hill C. E. Hypoxia-Inducible Factor 1α (HIF-1α) Counteracts the Acute Death of Cells Transplanted into the Injured Spinal Cord.eNeuro, 2020, vol. 7, no. 3, pp. 1–17.

Опубликован
2021-04-01
Как цитировать
Пастушенко, В., Кузнецов, М., Дворянчиков, В., Пастушенко, А., & Габаева, М. (2021). Mechanism of antisurdant action of triazin-indole derivative at experimental acoustic trauma. Вестник Санкт-Петербургского университета. Медицина, 16(1), 13–19. https://doi.org/10.21638/spbu11.2021.102
Раздел
Патологическая физиология