Abstract
Preclinical studies conducted so far suggest that oxidative stress processes may be associated with the mechanism of depression development. This study shows the effects of chronic administration of agomelatine on expression and the methylation status of Sod1, Sod2, Gpx1, Gpx4, Cat, Nos1, and Nos2 in the brain stricture and blood in the chronic mild stress (CMS) animal model of depression. The animals were exposed to the CMS procedure and treatment with agomelatine (10 mg/kg/day, IP) for five weeks and then were sacrificed. TaqMan Gene Expression Assay, Western blot, and methylation-sensitive high-resolution melting techniques were used to evaluate mRNA and protein expression of the genes, and the methylation status of their promoters. Gpx1, Gpx4, and Sod2 expression in the PBMCs and Sod1 and Sod2 expression in the brain were reduced in the stressed group after agomelatine administration. CMS caused an increase in the methylation of the third Gpx4 promoter in peripheral blood mononuclear cells and Gpx1 promoter in the cerebral cortex. Additionally, stressed rats treated with agomelatine displayed a significantly lower Gpx4 level in the hypothalamus. The results confirm the hypothesis that the CMS procedure and agomelatine administration change the expression level and methylation status of the promoter region of genes involved in oxidative and nitrosative stress.
Highlights
Depression is a common and serious mental disorder
Correlation between Differences in Sucrose Intake of Rats Subjected to Stress and Agomelatine
Sucrose of Rats Subjected to Stress and Agomelatine
Summary
Depression is a common and serious mental disorder. According to a report by the World HealthOrganization, 350 million people suffer from depression globally. 800,000 people in the world commit suicide every year [1,2]. Previous studies have shown that antioxidant disturbances play an important role in the. Genes 2020, 11, 644 pathogenesis of neurological and psychiatric diseases, depression [3]. This may be due to the fact that brain has a lower antioxidant capacity than other organs and is more sensitive to oxidative disorders [3]. A post-mortem study had shown an increased level of prooxidative enzyme, xanthine oxidase, in the serum and thalamus [18,19]
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