Neuroprotective effects of hyperoside, under conditions of mitochondrial complex IV activity deficiency
- Authors: Pozdnyakov D.I1
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Affiliations:
- Pyatigorsk Medical and Pharmaceutical Institute - branch of Volgograd State Medical University
- Issue: Vol 25, No 8 (2022)
- Pages: 48-52
- Section: Articles
- URL: https://journals.eco-vector.com/1560-9596/article/view/112983
- DOI: https://doi.org/10.29296/25877313-2022-08-06
- ID: 112983
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Abstract
Relevance. Neuroprotection is one of the significant components of the therapy of the central nervous system diseases which are associated with a violation of energy metabolism. The immediate cause of the deficiency of the intracellular pool of macroergic compounds may be the dysfunction of the mitochondrial complex IV. Hyperoside is a flavonoid with an extensive spectrum of pharmacological activity, including potentially high neuroprotective properties. Material and methods. Mitochondrial complex IV activity deficiency was modeled in Wistar rats by intracerebral injection of 3M sodium azide solution, an inhibitor of mitochondrial complex IV. Hyperoside and the reference drug ethylmethylhydroxypyridine succinate were administered orally at a dose of 100 mg / kg, for 30 days from the moment of injection of sodium azide. After that, the intensity of pyruvate-dependent cellular respiration and changes in the concentration of mitochondrial hydrogen peroxide in the brain tissue of animals were evaluated. Results. In the course of the work, it was found that the course administration of hyperoside and a reference drug contributed to an increase in the intensity of cellular respiration, which was expressed in an increase in ATP-generating activity, the maximum level of respiration and respirometric capacity in relation to untreated animals. Also, the use of the referent and hyperoside contributed to a statistically significant (p<0.05) decrease in the content of mitochondrial hydrogen peroxide, while more pronounced changes were obtained when hyperoside was administered to animals. Conclusion. The obtained results indicate that the course administration of hyperoside in conditions of energy deficiency caused by mitochondrial complex IV deficiency increases the intensity of cellular respiration processes and prevents the generation of reactive oxygen species, which in turn may be evidence of the presence of neuroprotective action.
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About the authors
D. I Pozdnyakov
Pyatigorsk Medical and Pharmaceutical Institute - branch of Volgograd State Medical University
Author for correspondence.
Email: pozdniackow.dmitry@yandex.ru
Ph.D. (Pharm.), Head of the Laboratory of Living Systems, Associate Professor of the Department of Pharmacology with a Course of Clinical Pharmacology
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