| Abstrakt: |
Introduction: At present, the issue of gastric mucosal damage, induced by the use of nonsteroidal anti-inflammatory drugs, remains unresolved. Objectives: The development of new methods of prevention of NSAID-gastropathies with oral coursework use of taurine and procaine, as well as the study of cellular mechanisms of the damaging effect of diclofenac sodium and Ketorolac tromethamine. Methods: The methodological approach was based on a range of theoretical, pharmacological, histological, statistical, biophysical methods. Results and discussion: Diclofenac sodium and ketorolac tromethamine, being in direct contact with cell membranes, cause a change in the structural and functional properties that present in the defect formation. This resulted in a decrease in the acid and hypo-osmotic resistance of model cells due to the broken or weakened bonds stabilizing the proteins molecules in membrane (which is associated with the dissociation of NH+-groups of the imidazole ring of histidine, the terminal α-amino groups (not less than 10.5% relative to the control), sulfhydryl groups of cysteine, phenolic groups of tyrosine, ε-amino groups of lysine (not less than 8.7%)). In experiments in vitro and in vivo procaine reduces the damaging effect of Ketorolac trometamina 28% and 19.7%, respectively, the formation of hidden defects reduced by 69% when taurine cellular damage was reduced by 54% and 19.7% of the latent defects is less than 74%. Conclusion: Prophylactic intragastric administration of procaine or taurine for 7 days before ketorolac tromethamine administration significantly reduces the amount of erosive and ulcerative defects (87% and 90%, respectively). [ABSTRACT FROM AUTHOR] |
