The Effect of Green Tea Polyphenols on the Change in the Mitochondrial Function of Hippocampal Cells in a Deficiency in the Activity of Mitochondrial Complex Iv

Abstract

The aim of the study was to evaluate the effect of green tea polyphenols on changes in the mitochondrial function in conditions of cerebrospecific blockade of mitochondrial complex IV activity. Materials and methods. Male Wistar rats were used in the work, in which the deficiency of mitochondrial complex IV activity was reproduced by direct injection of a 3M sodium azide solution into the hippocampal tissue. Green tea polyphenols and the reference drug ethylmethylhydroxypyridine succinate were administered at the dose of 100 mg/ kg, orally, for 30 days. Subsequently, changes in cognitive deficits in the Y-shaped maze test, the activity of succinate dehydrogenase and cytochrome-c-oxidase in hippocampal tissue were evaluated in rats. Results and their discussion. It was found that in animals without pharmacological support, when sodium azide was administered, there was a decrease in the activity of succinate dehydrogenase and cytochrome-c-oxidase by 29.2% (p < 0.05) and 78.8% (p < 0.05) with a deterioration in the rats' cognitive abilities by 47.6% (p < 0.05). the use of the reference drug and green tea polyphenols increased the activity of succinate dehydrogenase by 30.5% (p < 0.05) and 24.1% (p < 0.05), as well as that of cytochrome c oxidase by 20.9% (p < 0.05) and 56.0% (p < 0.05), respectively. the cognitive deficit in animals which received ethylmethylhydroxypyridine succinate and green tea polyphenols was significantly lower than that in untreated animals. Conclusions. Against the background of sodium azide introduction into the hippocampal tissue of animals, the development of cognitive deficits with a decrease in the activity of succinate dehydrogenase and cytochrome c oxidase is observed. a course administration of green tea polyphenols and a reference drug increased the activity of succinate dehydrogenase and cytochrome-c-oxidase, which contributed to the restoration of cognitive abilities in animals.

Correction of mitochondrial dysfunction with trimethoxy-substituted monocarbonyl curcumin analogues in experimental Alzheimer’s disease

“…The oxygen consumption was recorded on a laboratory respirometer AKPM 1-01L (Alfa-Bassens, Russia) and expressed in ppm/mg of protein, the content of which was determined by the Bradford method. The reagents used for the resprirometric analysis were provided by Sigma-Aldrich (Germany) [20,21].…”