PSIX-17 Cytokine profile of cow blood in the treatment of acute postpartum endometritis with recombinant α -, γ-interferons

Abstract

Abstract The aim of the study was to research the cytokine profile of cow blood in the treatment of acute postpartum endometritis with the use of recombinant α-, γ-interferons. Animals of the first group (n = 9) with a diagnosis of acute postpartum endometritis were intramuscularly injected with propranolol hydrochloride, denatured emulsified placenta, and nioxityl. Propranolol hydrochloride was administered for 4 days at a dose of 10 ml/animal at 24-hour intervals. The denatured emulsified placenta was injected subcutaneously on days 1-5-9 at a dose of 25 ml /animal. Nioxityl was injected intrauterine at a dose of 150 ml three times with a 48-hour interval. Cows of the second group (n = 11) with the same diagnosis were additionally injected intramuscularly with bovine recombinant α-, γ-interferons three times in 1–3 days at a dose of 5 ml/animal, 1 cm3 of which contains at least 1x104 IU/cm3 of the total antiviral activity of bovine recombinant α-, γ-interferons. Blood samples are taken from all groups before and at the end of the experiment. Blood samples are examined for the content of interleukin-2 (IL-2), interleukin-4 (IL-4), tumor necrosis factor alpha (TNFα), interleukin-10 (IL-10) using Bovine Elisa Kit Clood-Clone Corp (USA). The therapeutic effectiveness in the first group was 77.8%, in the second - 90.9%, which is 13.1% more. At the end of the course, the level of IL-2 decreased by 42.5% (43.5±4.2 pg/ml, P < 0.01), TNF-Α by 9.1% (457.9±34.6 pg/ml), the level of IL-4 increased by 14.8% (44.2±3.5 pg/ml, P < 0.05), IL-10 by 56.6% (35.7±2.8 pg/ml, P < 0.01). In the second group, the level of anti-inflammatory cytokines decreased: IL–2 by 48.7% (38.8±1.6 pg/ml, P < 0.01), TNFα by 26% (372.5±17.6 pg/ml, P < 0.05) and increased anti–inflammatory cytokines: IL-4 by 46.2% (56.3±4.1 pg/ml, P < 0.001) and IL-10 by 80.3% (41.1±3.5 pg/ml, P < 0.001), which indicates a decrease in the inflammatory response.