ABSTRACT
Data on the mechanisms of afobazole effect on the NO-producing function of endothelium under conditions of oxidative stress in rats with experimental diabetes mellitus are presents. It is established for the first time that the drug in vivo inhibits the intensity of lipid peroxidation, reduces the concentration of malonic dialdehyde in red blood cells up to 16.07% (p = 0.05), increases superoxide dismutase activity by 13.6% (p = 0.05), and increases the total concentration of nitric oxide metabolites in blood serum by 33.3% (p = 0.001). The drug effect on NO-producing function of endothelium is due to the increased availability of L-arginine to NO-synthase (NOS-3), reduced level of atherogenesis risk factor (LDL cholesterol in serum), and increased expression of NOS-3 in vascular endothelium on the average by 30.5% (p = 0,001).
