ПРОТИВОЯЗВЕННАЯ АКТИВНОСТЬ ДИНИТРАТА 2-ФЕНИЛ-9-ДИЭТИЛАМИНОЭТИЛИМИДАЗО[1,2-А]БЕНЗИМИДАЗОЛА ПРИ ГЕЛИКОБАКТЕРОПОДОБНОМ ПОВРЕЖДЕНИИ СЛИЗИСТОЙ ОБОЛОЧКИ ЖЕЛУДКА

The search for new drugs providing effective and safe therapy of acid-dependent diseases of the gastrointestinal tract, continues to be an actual problem of modern pharmacotherapy. One of the most significant pathogenetic mechanisms of these diseases is associated with Helicobacter pylori damage to the gastric mucosa. The aim of this study is the experimental investigation of the antiulcer effect of 2-phenyl-9-diethylaminoethylamine [1,2-a] benzimidazole substance (hereinafter a Benzimidazole derivative substance) on the model of Helicobacter pylori-like gastric mucosal injury in combination with immobilization stress (a restraint). Materials and methods. For modeling a mucous membrane damage to experimental animals (white Wistar male rats), they were injected 120 mmol/l ammonia solution after a 24-hour immobilization stress (restraint). As reference drugs, the following officinal anti-ulcer drugs widely used in clinical practice, had been chosen: Rranitidine (30 mg/kg, 10 mg/kg and 3 mg/kg) and Omeprazole (3 mg/kg, 1 mg/kg and 0.3 mg/kg). The study substance was used in the doses of 30 mg/kg, 10 mg/kg and 3 mg/kg. The maximum doses of the reference drugs were calculated on the basis of maximum daily doses for humans, taking into consideration the interspecies conversion factor. The maximum dose of the substance under study was selected experimentally. The logarithmic dose range was used for the convenience of further calculations of the ED 50 value. All the studied objects were introduced intragastrically through a non-traumatic tube. Results and discussion . It has been established that the studied substance significantly reduced the area of mucosal damage relative to the control values in modeling Helicobacter pylori-like gastric mucosal injury provoked by the administration of ammonia solution against the background of gastric mucosal ischemia after a 24-hour restraint. At the same time, the inhibition of ulceration reached 78%, while in the groups receiving Ranitidine and Omeprazole, it reached 66% and 50%, respectively. The calculated ED 50 values were the following: for the substance under study – 16.03 mg/kg, and for Ranitidine – 15.99 mg/kg. Conclusion. The gained results indicate that the studied Benzimidazole derivative is superior to analogs in its ability to suppress gastric mucosal ulceration provoked by Helicobacter pylori-like gastric mucosal injury, which confirms the relevance of further study of anti-ulcer activity and the development of the pharmaceutical dosage form based on it.