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On the Mechanism of the Cardioprotective Action of σ1 Receptor Agonist Anxiolytic Fabomotizole Hydrochloride (Afobazole)

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Original translational rat model of chronic heart failure provoked by experimental anterior transmural myocardium infarction was employed to examine the preventive action of anxiolytic Afobazole (15 mg/kg/day administered intraperitoneally during the first 15 days after coronary occlusion) on the development of the heart failure assessed in 3 months after infarction. Afobazole prevented the development of pathologic remodeling of the myocardium, maintained its inotropic function, and decreased the plasma level of brain natriuretic peptide known as a biochemical marker of chronic heart failure. In the myocardium, Afobazole down-regulated overexpression of the genes induced in chronic heart failure and assessed by corresponding RNA levels, which code angiotensin (AT1A-R), vasopressin (V1A-R), and glucocorticoid (GR) receptors as well as Epac2 protein. The revealed biochemical changes are consistent with the data on cardioprotective action of Afobazole.

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Correspondence to S. A. Kryzhanovskii.

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Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 165, No. 5, pp. 605-609, May, 2018

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Kryzhanovskii, S.A., Kozhevnikova, L.M., Tsorin, I.B. et al. On the Mechanism of the Cardioprotective Action of σ1 Receptor Agonist Anxiolytic Fabomotizole Hydrochloride (Afobazole). Bull Exp Biol Med 165, 660–664 (2018). https://doi.org/10.1007/s10517-018-4236-1

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  • DOI: https://doi.org/10.1007/s10517-018-4236-1

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