THE CONTENT OF PROSTANOIDS AND CYCLOOXYGENASES IN COLON TISSUE IN EXPERIMENTAL ULCERATIVE COLITIS

Introduction. The article examines changes in the content of prostaglandins and cyclooxygenases (COX) in colon tissue in ulcerative colitis induced by 2,4-dinitrobenzene sulfonic acid (DNBS) in a 50% ethanol solution. Based on the obtained results, the authors conclude that changes in the content of the studied parameters, except PGI2, are due to ethanol effect, not DNBS. Both COX isozymes are expressed in normal colon and reduced in ulcerative colitis. The aim. To study the prostanoids (PGE2, PGI2, PGF2α, TBX2 and 8-iso-PGF2α) and COX-1 and -2 contents in colon tissue in experimental ulcerative colitis. Materials and methods. The determination of prostanoids and cyclooxygenases contents in colon tissue by enzyme immunosorbent assay was carried out on three groups of sexually mature laboratory rats of both sexes of the WAG population (1st control group – intrarectal injection of saline; 2nd control group – injection of 50% ethanol; experimental group – injection of DNBS in 50% ethanol). Results. PGE2 and PGI2 contents in colon tissue of experimental group rats were statistically significantly higher compared 1st and 2nd control groups. The content of PGE2 was also increased in 2nd control group versus 1st control one. The increasing PGI2 in 2nd control group versus 1st control was not significant. TBX2 and PGF2α contents in experimental and 2nd control groups were significantly lower compared 1st control. 8-iso-PGF2α (non-enzymatically derived prostanoid) level in experimental group rats was significantly higher compared both controls. 8-iso-PGF2α content in 2nd control group was significantly higher compared 1st one. The content of both COX isoforms in colon tissue in experimental group and 2nd control group rats was significantly lower compared to 1st control group. Conclusions. Both isoforms of COX are expressed in control group colon indicating COX-2 involvement in supporting physiological functions of normal colon tissue. All studied indicators changes, except PGI2, are due to ethanol, not DNBS. Both 50% ethanol and DNBS in 50% ethanol stimulate lipid peroxidation, confirmed by significant increase in 8-iso-PGF2α content. PGE2 and PGF2α contents changes against the background of reduced levels of COX-1 and COX-2 in experimental ulcerative colitis are most likely an adaptive response aimed at maintaining colon homeostasis. PGI2 content changes are due to DNBS, and not to ethanol.