In cerebrovascular diseases dysfunction of central neuronal system functioning and the degree of pathophysiological and posthypoxic changes depends on activation of processes free radical oxidation and formation of “cytokine cascade” (ratio of proinflammatory and anti-inflammatory cytokines), that is why prospective chain in complex therapy of postischemic neurological complication in diabetes and stroke can be used cytokine drugs. The influence of the receptor antagonist IL-1 (RAIL-1) (7.5 mg/kg) on the changes of posthypoxic brain tissue (indexes of thiol-disulfide system, oxidative modification of proteins and energy metabolism) under modeling of alloxan diabetes and photoinduced bilateral vascular thrombosis in rats. It has been established that the post-ischemic cerebral tissue damage in experimental animals models accompanied by two discordant displacements components of thiol-disulfide system (increase of levels of oxidized glutathione and thiols by a sharp decrease in their reduced forms as well as reduced enzyme activity of the thiol-disulfide — glutathione peroxidase and glutathione reductase) and a pool of high-energy phosphates (reduced levels of ATP and ADP on the background of marked increase of levels of AMP), as well as an increase in brain homogenate markers of oxidative modification of proteins — AFG and CFG. There determined differences in the dynamics of changes in experimental diabetes and focal stroke. It was proved that the course of administration of RAIL-1 contributed to the stabilization of thiol-disulfide equilibrium normalization activities of glutathione peroxidase and glutathione reductase, as well as indicators energetic metabolism and oxidative modification of proteins in the brain tissue of rats with experimental diabetes and focal stroke.
