Immunological aspects of experimental hepatopathy induced by carprophen acceptance

The article presents the results of experimental studies, the purpose of which was to study the participation of proinflammatory cytokine - tumor necrosis factor а - in the development of hepatopathy, resulting from prolonged use of carprofen. Simulation of NSAID-induced liver damage in non-linear white rats was performed by oral administration of carprofen in different doses. The role of tumor necrosis factor in the development of hepatopathy was determined in the study of the immunohistochemical expression of the receptor for tumor necrosis factor а (T№aR1) using antibodies TNFR1. Histological examination of the liver tissue revealed changes characteristic of toxic damage, and the degree of liver tissue damage depends on the dose of the drug. High expression of T№aR1 in liver tissue is observed in animals of the experimental groups receiving a therapeutic and double dose of caprofen, which indicates that hepatocytes are ready for apoptosis due to the action of cytokine. Reduced expression of T№aR1 in experimental animals treated with high doses of the drug is associated with damage to the hepatocyte membrane and the predominance of necrosis in the liver parenchyma.