Нажмите на эту строку чтобы перейти к Новостям сайта "Русский врач"

Перейти
на сайт
журнала
"Врач"
Перейти на сайт журнала "Медицинская сестра"
Перейти на сайт журнала "Фармация"
Перейти на сайт журнала "Молекулярная медицина"
Перейти на сайт журнала "Вопросы биологической, медицинской и фармацевтической химии"
Журнал включен в российские и международные библиотечные и реферативные базы данных

ВАК (Россия)
РИНЦ (Россия)
Эко-Вектор (Россия)

OXYCINNAMIC ACIDS AS NOX4 INHIBITORS IN ALZHEIMER'S DISEASE THERAPY. AN EXPERIMENTAL STUDY

DOI: https://doi.org/10.29296/25877313-2023-06-07
Issue: 
6
Year: 
2023

D.I. Pozdnyakov
Ph.D. (Pharm.), Head of Living System Laboratory, Associate Professor,
Department of Pharmacology with Clinical Pharmacology Course, Pyatigorsk Medical and Pharmaceutical Institute (Pyatigorsk, Russia)
E-mail: pozdniackow.dmitry@yandex.ru

Relevance. Alzheimer's disease is a terminal form of dementia with a complex pathogenesis in which NOX-dependent oxidative stress plays an ex-tremely important role. Aim of the study. To evaluate the influence of oxycinnamic acids on the alteration of NOX4 activity in brain tissue of animals with experimental Alz-heimer's disease. Material and methods. Alzheimer's disease was modeled in Wistar rats by injection of β-amyloid aggregates with amino acid sequence 1-42 into hippocampal tissue (CA1 segment). Oxycinnamic acids: caffeic acid, coumaric acid, ferulic acid and synapic acid were administered at a dose of 100 mg/kg, orally for 60 days after the Alzheimer's disease model. Ethylmethylhydroxypyridine succinate was used as a reference drug in a similar dosage and dosing mode. Changes in the concentration of active NOX4 isophrome, hydrogen peroxide as well as β-amyloid in brain tissue of rats were as-sessed after the indicated time period. Results. This study showed that the analyzed oxycinnamic acids were comparable with each other and the referent. Thus, a statistically significant (p

Keywords: 
Alzheimer's disease
NOX4
β-amyloid
oxidative stress
oxycinnamic acids.

References: 
  1. Khan S., Barve K.H., Kumar M.S. Recent Advancements in Patho-genesis, Diagnostics and Treatment of Alzheimer's Disease. Curr Neuropharmacol. 2020; 18(11): 1106–1125.
  2. Scheltens P., De Strooper B., Kivipelto M., Holstege H., Chételat G., Teunissen C.E., Cummings J., van der Flier W.M. Alzheimer's disease. Lancet. 2021; 397(10284): 1577–1590.
  3. Oren O., Taube R., Papo N. Amyloid β structural polymorphism, associated toxicity and therapeutic strategies. Cell Mol Life Sci. 2021; 78(23): 7185–7198.
  4. Cheignon C., Tomas M., Bonnefont-Rousselot D., Faller P., Hureau C., Collin F. Oxidative stress and the amyloid beta peptide in Alzheimer's disease. Redox Biol. 2018; 14: 450–464.
  5. Tarafdar A., Pula G. The Role of NADPH Oxidases and Oxidative Stress in Neurodegenerative Disorders. Int J Mol Sci. 2018; 19(12): 3824.
  6. Wang K., Shi J., Zhou Y., He Y., Mi J., Yang J., Liu S., Tang X., Liu W., Tan Z., Sang Z. Design, synthesis and evaluation of cinnamic acid hybrids as multi-target-directed agents for the treatment of Alz-heimer's disease. Bioorg Chem. 2021; 112: 104879.
  7. Manczak M., Reddy P.H. Abnormal interaction between the mito-chondrial fission protein Drp1 and hyperphosphorylated tau in Alz-heimer's disease neurons: implications for mitochondrial dysfunc-tion and neuronal damage. Hum Mol Genet. 2012; 21(11): 2538–2547.
  8. Воронков А.В., Поздняков Д.И., Аджиахметова С.Л., Червон-ная Н.М., Руковицина В.М., Оганесян Э.Т. Влияние некоторых производных коричной кислоты на изменение активности фер-ментов цикла трикарбоновых кислот у крыс в условиях ише-мии головного мозга. Медицинский академический журнал. 2020; 20(2): 27–32 [Voronkov A.V., Pozdnjakov D.I., Adzhiahmetova S.L., Chervonnaja N.M., Rukovicina V.M., Ogan-esjan Je.T. Vlija-nie nekotoryh proizvodnyh korichnoj kisloty na iz-menenie aktivnosti fermentov cikla trikarbonovyh kislot u krys v uslovijah ishemii golovnogo mozga. Medicinskij akademicheskij zhurnal. 2020; 20(2): 27–32 (in Russ)].
  9. Summers F.A., Zhao B., Ganini D., Mason R.P. Photooxidation of Amplex Red to resorufin: implications of exposing the Amplex Red assay to light. Methods Enzymol. 2013; 526: 1–17.
  10. Butterfield D.A. The 2013 SFRBM discovery award: selected dis-coveries from the butterfield laboratory of oxidative stress and its sequela in brain in cognitive disorders exemplified by Alzheimer disease and chemotherapy induced cognitive impairment. Free Rad-ic Biol Med. 2014; 74: 157–74.
  11. Wang X., Wang W., Li L., Perry G., Lee H.G., Zhu X. Oxidative stress and mitochondrial dysfunction in Alzheimer's disease. Bio-chim Biophys Acta. 2014; 1842(8): 1240–1247.
  12. Luengo E., Trigo-Alonso P., Fernández-Mendívil C., Nuñez Á., Campo M.D., Porrero C., García-Magro N., Negredo P., Senar S., Sánchez-Ramos C., Bernal J.A., Rábano A., Hoozemans J., Casas A.I., Schmidt H.H.H.W., López M.G. Implication of type 4 NADPH oxidase (NOX4) in tauopathy. Redox Biol. 2022; 49: 102210.