Introduction. Radiation injury of the bladder is a complication after therapeutic irradiation of the pelvic organs. The strategy of pharmacotherapy of such complications is currently unclear due to the small number of studies and unclear pathogenesis.

Purpose of the study – to study the effectiveness of the use of bovine bladder polypeptides in modeling radiation injury of the bladder in rats.

Materials and methods. An animal model of radiation cystitis was formed by a single irradiation at a dose of 20 Gy with determination of the isocenter on a 3D model. The study used 55 female Wistar rats, which were divided into 5 groups: group 1 – intact, without exposure; group 2 – negative control (irradiation without therapy); group 3 – therapy with Vezusten, starting from the 10th day after irradiation, intramuscularly daily for 10 days, at a dose of 0.056 mg/kg, in a volume of 0.1 ml; Group 4 – administration of Vezusten to intact animals, intramuscularly daily for 10 days, at a dose of 0.056 mg/kg, in a volume of 0.1 ml; Group 5 – «standard therapy» was administered, instillation of a combination of hydrocor- tisone+heparin+lidocaine for 10 days, starting from the 10th day after irradiation. The animals were withdrawn on the 40th day after irradiation. Results. In the achieved model of radiation cystitis, in the group receiving the peptide drug Vezusten, much less damage to the bladder wall was noted (preservation of epithelial stratification, folding, plethora of the submucosal layer), as well as better tolerance of irradiation and the post-radiation period (less pronounced alopecia, minimal skin changes in the places of animal fixation, physiological behavior of the animal).

Conclusion. In the achieved experimental model of radiation cystitis in rats, the introduction of regulatory polypeptides of the urinary bladder of cattle (the drug Vezusten) significantly reduced both the clinical manifestations of radiation injury and normalized the morphological picture. Probably, the reparative effect of Vezusten is realized, among other things, due to the normalization of the expression of the paracrine peptide factor TGF-β1, compared to animals without therapy.