ASSESSMENT OF THE INFLAMMATORY RESPONSE IN THE PANCREAS AFTER ADMINISTRATION OF N-ACETYL CYSTEINE IN A MODEL OF POST-RADIATION PANCREATITIS

Introduction. Ionizing radiation can lead to radiation damage to healthy pancreatic tissue, with the development of signs of post-radiation pancreatitis. Electron irradiation potentially has the most “sparing” effect on healthy tissue, but data on this are sparse. The search for means to protect healthy tissues from the effects of ionizing radiation remains relevant. Thus, the use of agents with antioxidant properties (N-acetylcysteine) can potentially slow down the development of post-radiation pancreatitis. The aim of the study: assessment of the inflammatory response in the pancreas after administration of N-acetylcysteine in a radiation-induced pancreatitis model. Methods. Wistar rats (n=120) were divided into four groups: I (n=30) – control; II (n=30) – irradiation with electrons in a total irradiation dose of 25 Gy; III (n=30) – pre-irradiation administration of N-acetylcysteine before electron irradiation; IV (n=30) – administration of N-acetylcysteine. Animals were removed from the experiment on the 7th, 30th and 90th days. A morphological assessment of pancreatic fragments and an immunohistochemical study with antibodies to pro- (IL-1, IL-6) and anti-inflammatory (IL-10) cytokines, markers of T-lymphocytes (CD3) and macrophages (CD68) were carried out. Results. At all stages of the experiment, high levels of expression of pro- and anti-inflammatory cytokines were observed in the electron irradiation group with a slight increase in the number of CD3+ T-lymphocytes and CD68+ macrophages. In the group of pre-radiation administration of N-acetylcysteine, increased levels of immunolabeling were also found when conducting reactions with antibodies to pro- and anti-inflammatory cytokines, however, by the third month of the experiment, practically no CD3+ and CD68+ immunocompetent cells were noted in this group. Conclusion. Pancreatic local electron irradiation at a total dose of 25 Gy in the early stages leads to the development of a stromal-vascular inflammatory reaction with a capillary-parenchymal block with practically no cellular inflammatory infiltration. At the same time, pre-radiation administration of N-acetylcysteine partially prevents the development of post-radiation pancreatitis.