Publication: Comparison of the protective effects of lansoprazole and omeprazole against acetyl salicylic acid-induced gastric damage in rats
Abstract
Omeprazolun antisekretuvar ve antioksidan özellikleriyle, asetilsalisilik asit (ASA) ile oluşturulan gastrik mukozal hasara karşı koruyucu etkileri olduğu bildirilmiştir. Bu çalışmanın amacı lansoprazolun artan dozlarının antisekretuar ve antioksidan etkilerini incelemek ve bu etkileri omeprazol ile karşılaştırmaktır. Gastrik lezyonlar aç bırakılan hayvanlarda ASA (200 mg/kg)- uygulaması ile oluşturuldu. Çalışma 5 grupta yapıldı; Kontrol, Açlık, ASA, Omeprazol (20, 40, 80 (mol/kg) + ASA, ve Lansoprazol (1, 5, 10 mg/kg) + ASA. Mukozal hasar, gastrik asit, lipid peroksidasyonu (LPO), glutatyon (GSH) ve myeloperoksidaz (MPO) aktivitesi tayinleri yapıldı. Her iki ilaç da ASA ile oluşturulan gastrik ülseri önemli ölçüde önledi. ASA'ın neden olduğu gastrik asit, LPO ve MPO artışlarını azalttı, ve azalan GSH düzeylerini yükseltti. Bu sonuçlara göre artan asidite kadar reaktif oksijen türevleri ve lipid peroksidasyonu ASA ile oluşturulan gastrik hasarın patogenezinde önemli rol oynamaktadır, incelenen bu ilaçların gastrik hasara karşı koruyucu etkilerinin onların antioksidan özellikleri ve asit sekresyonunu inhibe edici özellikleri ile ilgili olabileceği görülmektedir.
Omeprazole and lansoprazole have been reported to be protective against acetylsalicylic acid (ASA) induced gastric mucosal injury due to their proton pump (K+/H+-ATPase) inhibitor properties. The aim of this study was; to investigate the antisecretory, and the antioxidant effects of increasing doses of lansoprazole and also compare them with those of omeprazole against ASA-induced gastric damage in rats. Gastric lesions were induced by administration of ASA (200 mg/kg) to fasted rats. Studies were performed on five groups of animals; control, starvation, ASA, Omeprazole (20, 40, 80 (mol/kg) + ASA and Lansoprazole (1, 5, 10 mg/kg) + ASA groups. Mucosal damage, gastric acidity, as well as lipid peroxidation (LPO), glutathione (GSH) levels and myeloperoxidase (MPO) activity were determined . Both drugs significantly prevented the gastric ulcerogenesis induced by ASA, decreased the ulcer index, and the gastric acidity dose dependently. LPO, and MPO activities, which were increased by ASA, were decreased, and the GSH levels, which were decreased, were increased significantly. According to these findings, as well as the increased acidity, active oxygen species and LPO also play an important role in the pathogenesis of ASA-induced gastric damage. The drugs studied may be protective against this damage due to their antioxidant properties, and also by inhibition of acid secretion.
Omeprazole and lansoprazole have been reported to be protective against acetylsalicylic acid (ASA) induced gastric mucosal injury due to their proton pump (K+/H+-ATPase) inhibitor properties. The aim of this study was; to investigate the antisecretory, and the antioxidant effects of increasing doses of lansoprazole and also compare them with those of omeprazole against ASA-induced gastric damage in rats. Gastric lesions were induced by administration of ASA (200 mg/kg) to fasted rats. Studies were performed on five groups of animals; control, starvation, ASA, Omeprazole (20, 40, 80 (mol/kg) + ASA and Lansoprazole (1, 5, 10 mg/kg) + ASA groups. Mucosal damage, gastric acidity, as well as lipid peroxidation (LPO), glutathione (GSH) levels and myeloperoxidase (MPO) activity were determined . Both drugs significantly prevented the gastric ulcerogenesis induced by ASA, decreased the ulcer index, and the gastric acidity dose dependently. LPO, and MPO activities, which were increased by ASA, were decreased, and the GSH levels, which were decreased, were increased significantly. According to these findings, as well as the increased acidity, active oxygen species and LPO also play an important role in the pathogenesis of ASA-induced gastric damage. The drugs studied may be protective against this damage due to their antioxidant properties, and also by inhibition of acid secretion.