Mitochondrial dysfunction is a universal pathogenetic mechanism that plays an essential role in ischemic brain damage. At the same time, the study of mitochondrial biogenesis will significantly improve the effectiveness of targeted therapeutic effects on the mitochondria of the cell.
The aim of the study was to evaluate changes in mitochondrial biogenesis in rat brain tissue under conditions of permanent focal ischemia.
Material and methods. Cerebral ischemia was modeled in male rats by irreversible right-sided coagulation of the middle cerebral artery. Mitochondrial biogenesis was assessed by changes in the activity of succinate dehydrogenase and cytochrome-c oxidase in rats in the dynamics by the spectrophotometric method. Also, in rats, the change in the size of the brain necrosis zone was determined by the degree of recovery of formazan triphenyltetrazolium chloride.
Results. The study showed that the most pronounced changes in the activity of succinate dehydrogenase and cytochrome-c oxidase were noted 72 hours after the simulation of ischemia. At the same time, in comparison with sham-operated animals, the activity of enzymes decreased by 53.1% (p<0.05) and 60% (p<0.05), respectively. It is worth noting that changes in the enzymatic activity of succinate dehydrogenase and cytochrome-c oxidase correlated with an increase in the brain necrosis zone with the values of correlation coefficients r=0.71324 and r=0.83629, respectively.
The authors declare no conflicts of interest.
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