ASSESSMENT OF INFLAMMATORY MARKERS IN RATS WITH EXPERIMENTALLY INDUCED ULCERATIVE COLITIS

Introduction. Inflammatory bowel diseases develop under the combined influence of endogenous and exogenous factors, leading to an uncontrolled inflammatory response of the intestinal mucosa. One of the key directions in studying their pathogenesis involves the assessment of changes in the levels of proinflammatory cytokines and enzymes. Determination of tumor necrosis factor α, matrix metalloproteinase activity, and lipopolysaccharide concentration serves as an informative approach for evaluating inflammation and destructive processes in the intestinal wall. Objective. The aim of the study was to assess the content of lipopolysaccharide, tumor necrosis factor α, and matrix metalloproteinase-9 activity as potential markers and activators of proinflammatory pathways in rats with experimental colitis induced by 2,4-dinitrobenzenesulfonic acid. Materials and methods. The study was conducted on eighteen adult male rats of the WAG strain (body weight 190–240 grams, age 4 months), kept under standard vivarium conditions. The animals were randomly divided into three groups of six. The first (control) group received 0.9 % physiological saline rectally, the second group received 50 % ethanol, and the third group was administered a solution of 2,4-dinitrobenzenesulfonic acid (10 milligrams dissolved in 250 microliters of 50 % ethanol) for fourteen days. The concentrations of lipopolysaccharide and tumor necrosis factor α and the activity of matrix metalloproteinase-9 in blood serum were measured using commercial enzyme-linked immunosorbent assay kits (Abbexa, United States; Labor Diagnostika Nord, Germany; Fine Test, Republic of Korea) on a Stat Fax 1904 microplate reader in accordance with the manufacturers’ protocols. Results. Rats with colitis induced by 2,4-dinitrobenzenesulfonic acid demonstrated a significant increase in serum levels of lipopolysaccharide and tumor necrosis factor α compared with both control groups. An elevation of these parameters was also observed in the ethanol control group, indicating its additional proinflammatory effect. The activity of matrix metalloproteinase-9 increased in both ethanol-treated and 2,4-dinitrobenzenesulfonic acid-treated animals; however, no statistically significant difference between these groups was detected. Conclusion. The observed elevation of lipopolysaccharide, tumor necrosis factor α, and matrix metalloproteinase-9 activity in the serum confirms activation of inflammatory mechanisms in colitis induced by 2,4-dinitrobenzenesulfonic acid. The findings suggest that 50 % ethanol alone may act as a mucosal-damaging agent and contribute to the enhancement of the intestinal inflammatory response.