Lectinocytochemical study of rat stomach mucosa under the conditions of cyclooxygenase-1/-2 blockage and pretreatment witH H-Glu-Asp-Gly-OH

Assessment of glycoconjugate expression on cell membranes using the lectin histochemistry technique may be a feasible approach for evaluating the functional state of the cell. The aim of this study was to evaluate carbohydrate determinants of rat stomach mucosa cell membranes under the conditions of COX-1/-2 blockage­ with indomethacin and pretreatment with the tripeptide H-Glu-Asp-Gly-OH. Male Wistar rats were divided into 3 groups (n = 6 per group): 1st group (control) received vehicle; 2nd – indomethacin (35 mg/kg); 3rd – H-Glu-Asp-Gly-OH (10 µg) 30 min before indomethacin. Rats were sacrificed 24 hours later. Gastric mucosa (GM) carbohydrate determinants were studied by lectin-peroxidase technique. The lectins panel included α-fucose- (LABA), syalo- (WGA, SNA), mannose- (Con A, LCA) and galactose-specific (HPA, PNA, SBA) lectins. Intensity of lectin-receptor reaction was scored: 0 – no reaction; 1 – weak; 2 – mild; and 3 – strong reaction. COX-1/2 blockage caused GM lesions, attenuated by H-Glu-Asp-Gly-OH. WGA and SNA showed the highest affinity to GM. Indomethacin decreased SNA-labeling of epitheliocytes and mucocytes and LABA-labeling of chief cells. H-Glu-Asp-Gly-OH reversed the glycosylation changes, caused by COX-1/COX-2 blockage only in regards to labeling of chief cells with LABA, epitheliocytes and mucocytes with LCA, mucocytes with SNA. Predominantly H-Glu-Asp-Gly-OH under COX-1/COX-2 blockage had an effect opposite to indomethacin alone but glycosylation changes under these conditions differed significantly also from the control. COX-1/COX-2 blockage causes alteration of glycosylation processes in rat GM, mainly reduction of NeuNAc(α2-6)DGal and α-Fuc content. H-Glu-Asp-Gly-OH under the conditions of COX-1/COX-2 blockage leads to more profound changes in GM lectin-binding pattern compared to the independent effect of indomethacin and to control.