The Study of Neuroprotective Mechanisms of the Ubiquinol Action in Experimental Focal Ischemia

Ischemic stroke is one of the most socially important diseases characterized by impaired cerebral circulation with focal damage of the brain tissue and decreased functionality. Despite the achievements of modern pharmacology, possibilities of pharmacotherapy of stroke remain limited, and the research for new drugs with neuroprotective effects that can prevent brain cell death still attracts much attention. In this study we have investigated the neuroprotective activity of ubiquinol used in a new innovative form for intravenous administration form on a rat model of permanent 24 h cerebral ischemia with evaluation of the mechanisms of its neuroprotective effect. Ubiquinol (30 mg/kg), administered intravenously in the acute period of permanent 24 h focal cerebral ischemia, had a direct neuroprotective effect, characterized by a decrease in the volume of brain tissue necrosis. The protective effect of ubiquinol was determined by its ability to inhibit the development of oxidative stress due to its direct anti-radical action, preventing the increase in the lipid hydroperoxide content in the brain tissue adjacent to the focus of necrosis, decreasing lipid oxidation rate in plasma under conditions of increased total antioxidant activity in the brain and blood of experimental animals. In vitro experiments have shown the ability of ubiquinol to prevent cell death in primary culture of rat cerebral cortex neurons under 4 h oxygen/glucose deprivation followed by 20 h reoxygenation.