The Effect of Mesedin on the Content of Oxidative Stress Biomarkers in the Brain Tissue in Ischemia

Abstract

The effect of α2-adrenoblocker mesedin (2-(2-methylamino-4-thiazolyl)-1,4-benzodioxane hydrochloride) on the content of oxidative stress biomarkers in the brain tissue was well studied in ischemic disorders. The aim of this study is to reveal the possible mechanisms of the antihypoxic effect of mesedin. The quantitative changes of the final product of lipid peroxidation (LP)—malondialdehyde (MDA) and carbonyl derivatives of proteins — aldehyde-dinitrophenylhydrazones of neutral character (ADNPuv), ketone-dinitro-phenylhydrazones of neutral character (KDNPuv), aldehyde-dinitrophenylhydrazones of basic character (ADNPvs) and ketone-dinitrophenylhydrazones of basic character (KDNPvs) were studied in the brain tissue of rats (n = 56) under the condition of experimental ischemia caused by the ligation of the right common carotid artery. The study showed that one of the possible mechanisms of antihypoxic action of mesedin is its ability to prevent the accumulation of malondialdehyde and to limit protein carbonylation in brain ischemia. The data received demonstrates that mesedin could serve as a potential medicine for the correction of cerebrovascular ischemic disorders, for the reason that along with improving cerebral blood flow and preventing the development of morphological shifts and neurobehavioral disturbances in brain local ischemia, the medicine also mitigates the aggressive action of oxidative stress while protecting the brain tissue from the consequences of hypoxia.