Abstract
Background. Acute disorders of cerebral blood circulation are one of the most important medical and social problems, due to their high share in the structure of morbidity and mortality of the population, significant indicators of temporary loss of working capacity and primary disability. At the same time, the World Health Organization estimates that by 2021, 615 million people (about 10% of the world's population) will have symptoms of depressive or anxiety disorders. Therefore, the study of the pathogenetic links of comorbidity of anxiety-depressive disorders against the background of ischemic stroke is relevant.
 Aim: to study changes in antioxidant protection and lipid peroxidation under conditions of experimental ischemic stroke comorbid with anxiety-depressive disorders.
 Materials and methods. Experimental studies were conducted on 30 non-linear laboratory rats, which were divided into 3 groups: 1 group – intact control, 2 group – animals of the group with simulated ischemic stroke; Group 3 – rats with simulated ischemic stroke and anxiety-depressive disorders. Reproduction of ischemic stroke in rats was carried out using the model of endovascular occlusion of the middle cerebral artery (focal ischemia) according to E. Z. Longa. A model of reserpine-induced depression in rats was chosen for an in-depth study of the pathophysiological links of anxiety-depressive disorders.
 To assess the state of lipid peroxidation and the antioxidant defense system, the level of malondialdehyde, catalase, superoxide dismutase, and reduced glutathione in brain tissue homogenate and circulating blood was studied.
 Results. A sharp depletion of the body's protective reactions was established in rats with both ischemic stroke and under conditions of comorbid pathology, which was confirmed by a probable decrease in the level of catalase, superoxide dismutase and an increased level of malondialdehyde. In particular, the level of catalase and superoxide dismutase decreased in the brain tissue homogenate of rats with comorbid pathology; the level of malondialdehyde increased. At the circulating level, there was a 40-fold increase in the level of catalase (p<0.05) compared to intact animals, which indicated a compensatory reaction of the body to the activation of free-radical oxidation, since this enzyme neutralizes hydrogen peroxide.
 Conclusions. The obtained data indicate a more severe course of ischemic stroke against the background of anxiety-depressive disorders and the involvement of both pro- and anti-inflammatory cytokines in the development mechanism, as well as a violation of the balance between the processes of lipid peroxidation and antioxidant protection.
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