The Effect of Ubiquinol on Cerebral Endothelial Cells in Different Regions of Rat Brain

The ability of the promising antioxidant and neuroprotective medicine coenzyme Q10 to penetrate the blood-brain barrier (BBB) makes it a potential agent that can influence the mitochondrial metabolism of brain cells. Its reduced form (ubiquinol) is of particular interest. It can affect the structural and functional activity of cells that form the BBB. However, the mechanisms of penetration, the drug effect on brain cells and its actions are not fully understood. The aim of our work was to study the effect of ubiquinol on regulating molecules of BBB permeability and apoptosis processes in various structures of the rat brain. The effect of coenzyme Q10 on the quantity of CD31, Pgp and CLDN5 immunopositive cells and on the level of apoptosis in sections of different parts of the rat brain after a single intravenous injection of ubiquinol at a dose of 30 mg/kg was evaluated. The results indicate that ubiquinol causes an increase in the quantity of cells carrying the CD31 marker in the entorhinal cortex within 2–24h after exposure, followed by an increase in CLDN5 within 96–192h after exposure. It is noteworthy that in the amygdala, an increase in CD31 was accompanied by a delayed decrease in CLDN5, while in the hippocampus we registered only a decrease in CLDN5. Our data on an apoptosis intensity decrease do not allow us to say what contribution to this effect is made by cerebral endotheliocytes. However, the revealed signs of intensification of angiogenesis and region-specific changes in the BBB integrity under the action of ubiquinol allow us to consider it as a promising agent for the correction of BBB dysfunction in brain diseases.