Pathogenetic Aspects Of Experimental Pancreatopathy Induced By Nimesulid

Abstract

Objective: to study the involvement of regulatory cytokine-interleukin-2 in the pathogenesis of NSAID-pancreatopathy induced by prolonged intake of nimesulide, using immunohistochemical methods. Materials and methods: the study was carried out on laboratory animals (rats) who received nimesulide by the oral route for 21 days at different dosages: 0.5 mg / kg (therapeutic), 2.5 mg / kg and 5 mg / kg. Evaluation of the effect of the drug was made on the basis of histological examination of pancreatic tissue and manifestation of immunohistochemical expression of interleukin-2 (IL-2Rα) receptors. To identify the expression of receptors, labeled antibodies IL-2Rα (poly), species-specific to rat tissue antigens, were used. Results: histological studies revealed pathomorphological changes characteristic of toxic pancreatic lesions. Assessment of the degree of lesions showed a pronounced dose-dependent effect. The manifestation of immunohistochemical expression of IL-2Rα was determined by semi-quantitative methods, the intensity of staining and the number of positively stained cells were evaluated. It was found that the expression of IL-2Rα is localized in the endocrine islets of Langerhans. In animals of experimental groups receiving high doses of nimesulide, a significant increase in the intensity of staining of endocrine islets as well as connective tissue components was revealed, which is due to the high intensity of expression of IL-2Rα. Conclusion: increased expression of IL-2Rα, reflecting islet cell damage, may be due to deterioration of tissue nutrition of islands due to hemodynamic disorders and dystrophic processes in the parenchyma of the gland and the development of an autoimmune component of the inflammatory process.