Publication: Asetilsalisilik asit ile oluşturulan gastrik mukozal hasara karşı lansoprazol’ ün koruyucu etkisinin melatoninle karşılaştırılmalı olarak incelenmesi
Abstract
Peptik ülser tedavisinde kullanılan lansoprazol yeni bir proton pompası inhibitörü olup antisekretuar etkisi yanında sitoprotektif etkisi de olduğu ileri sürülmektedir. Daha önce diğer bir proton pompası inhibitörü olan omeprazol'ün güçlü antioksidan etkisi gösterilmiş olduğundan bu çalışmada da lansoprazol'ün asetilsalisilik asit (ASA) ile oluşturulan gastrik hasara karşı koruyucu etkisi ve bunun mekanizması güçlü bir antioksidan olan melatoninle karşılaştırmalı olarak incelenmiştir. Zira ASA'nın neden olduğu gastrik mukozal hasarın patogenezinde reaktif oksijen türlerinin ve lipid peroksidasyonunun önemli bir rol oynadığı ileri sürülmektedir. Çalışmamızda her iki cinsten wistar albino sıçanlar kullanılmış ve çalışma 5 grup hayvanda yapılmıştır. Kontrol (K) grubuna 3 saat, Açlık (A) grubuna ise 48 saat açlığı takiben pilor ligasyonu yapılmıştır. Ülser (Ü) grubu: 48 saat açlığı takiben ASA (200mg/ kg oral) uygulanmış ve 1 saat sonra pilor ligasyonu yapılmıştır. Lansoprazol (L) grupları: 48 saat aç bırakılan hayvanlara ASA uygulamasından 1 saat önce gavaj yoluyla lansoprazol (1mg/ kg (L1), 5 mg/ kg (L5 ), 10 mg/ kg (L10 ) oral) uygulanmış ve ASA uygulamasından 1 saat sonra pilor ligasyonu yapılmıştır. Melatonin (M) grubu: 48 saat aç bırakılan hayvanlara ASA uygulamasından 30 dakika önce 10mg/ kg melatonin uygulanmış ve yine ASA uygulamasından 1 saat sonra pilor ligasyonu yapılmıştır. Pilor ligasyonundan 2 saat sonra hayvanlar servikal dislokasyonla öldürülmüş mide sıvıları alınmış ve dokuda ülser indeksi, total asidite, malondialdehid ve glutatyon düzeyleri ile myeloperoksidaz aktivitesi incelenmiştir. Lansoprazol ve melatonin uygulanması ASA'ya bağlı olarak artan lipid peroksidasyonu (LPO) ve myeloperoksidaz (MPO) düzeylerini azaltırken glutatyon (GSH) düzeylerindeki azalmayı önlemişlerdir. Lansoprazol ASA'nın neden olduğu asidite artışını da dozla orantılı olarak azaltırken melatonin'in etkisi çok zayıftır.
COMPRASION OF THE PROTECTIVE EFFECTS OF MELATONIN AND LANSOPRAZOLE AGAINST ACETYLSALICYLIC ACID INDUCED GASTRIC MUCOSAL INJURY It has been proposed that the reactive oxygen species and lipid peroxidation have an important role in the pathogenesis of the gastric mucosal injury induced by acetylsalicylic acid (ASA). In this study we aimed to investigate the antiulcer and antioxidant properties of a new proton pump inhibitor lansoprazole in comparasion to melatonin in ASA induced gastric damage in rats. Study was performed on 5 groups of rats: Control (C ) groupStarvation ( S) group Ulcer ( U) group: After 48 hours of starvation, ASA (200mg/ kg) was administered orally, pyloric ligation was performed 1 hour later. Lansoprazole (L) (1, 5, 10 mg/ kg) groups: After 48 h of starvation, lansoprazole was administered orally 1 h before ASA, and pyloric ligation was performed 1 h after ASA. Melatonin (M) (10mg/ kg, i.p.) group: After 48 h of starvation melatonin was administered 30 min before ASA and pyloric ligation was performed 1 h after ASA. 2 h after pylor ligation rats were killed, stomachs were removed and gastric contents were taken out. As well as the macroscopic examination and the gastric acidity, glutathion, lipid peroxidation and myeloperoxidase levels of the gastric tissues were determined. It was observed that lansoprazole and melatonin considerably prevented ulcer formation and lansoprazole also suppressed the gastric acidity. LPO and MPO activities which were increased by ASA were decreased significantly by lansoprazole and melatonin and the decrease in GSH levels was prevented by lansoprazole and melatonin. Effect of lansoprazole on all of these parametres were dose dependent. Our results confirm that reactive oxygen species as well as acidity have a role in the pathogenesis of the gastric mucosal injury induced by ASA, and lansoprazole protects effects against this damage both by its antisecretory and antioxidant properties.
COMPRASION OF THE PROTECTIVE EFFECTS OF MELATONIN AND LANSOPRAZOLE AGAINST ACETYLSALICYLIC ACID INDUCED GASTRIC MUCOSAL INJURY It has been proposed that the reactive oxygen species and lipid peroxidation have an important role in the pathogenesis of the gastric mucosal injury induced by acetylsalicylic acid (ASA). In this study we aimed to investigate the antiulcer and antioxidant properties of a new proton pump inhibitor lansoprazole in comparasion to melatonin in ASA induced gastric damage in rats. Study was performed on 5 groups of rats: Control (C ) groupStarvation ( S) group Ulcer ( U) group: After 48 hours of starvation, ASA (200mg/ kg) was administered orally, pyloric ligation was performed 1 hour later. Lansoprazole (L) (1, 5, 10 mg/ kg) groups: After 48 h of starvation, lansoprazole was administered orally 1 h before ASA, and pyloric ligation was performed 1 h after ASA. Melatonin (M) (10mg/ kg, i.p.) group: After 48 h of starvation melatonin was administered 30 min before ASA and pyloric ligation was performed 1 h after ASA. 2 h after pylor ligation rats were killed, stomachs were removed and gastric contents were taken out. As well as the macroscopic examination and the gastric acidity, glutathion, lipid peroxidation and myeloperoxidase levels of the gastric tissues were determined. It was observed that lansoprazole and melatonin considerably prevented ulcer formation and lansoprazole also suppressed the gastric acidity. LPO and MPO activities which were increased by ASA were decreased significantly by lansoprazole and melatonin and the decrease in GSH levels was prevented by lansoprazole and melatonin. Effect of lansoprazole on all of these parametres were dose dependent. Our results confirm that reactive oxygen species as well as acidity have a role in the pathogenesis of the gastric mucosal injury induced by ASA, and lansoprazole protects effects against this damage both by its antisecretory and antioxidant properties.