The potential protective effects of Aliskiren on diclofenac sodium induced gastric ulcer in a rat model

Abstract

Introduction: Abrasion of stomach lining epithelium is caused by a defensive, protective mechanism, and aggressive factor imbalance. 20% of peptic ulcers begin as minor erosion of stomach lumen epithelia and extend to muscularis mucosa or submucosa 5 mm or larger. This research aims to minimise stomach mucosal lesions induced by NSAIDs by utilising Aliskiren. Method: 30 male albino rats were split into 4 groups. Negative control group A received 0.9% NaCl and tween 80 via oral gavage. Group B: Animals received ulcerogen (150 mg/kg Diclofenac sodium) orally and were not pre-treated. Group C: Diclofenac soduim and Omeprazole 20 mg/kg orally before ulcerogen. Group D received Diclofenac and Aliskierin via oral gavage before ulcerogen. Results: Diclofenac sodium at 150 mg/kg increases (p>0.01) stomach damage score, TNF-alpha expression, myeloperoxidase, malonaldehyde, and ulcer development % compared to healthy rats. Aliskierin 200 mg/kg pretreatment in Diclofenac-induced-ulcer in rats reduces (p>0.01) stomach damage score, TNF-alpha, myeloperoxidase, malonaldehyde, and ulcer formation percent, although less efficiently than Omeprazole and Aliskierin. Conclusion: Aliskierin inhibits Diclofenac. Aliskierin performed similarly to standard treatment (Omeprazole). Pirfenidone's protective effect was mostly due to its antioxidant and anti-inflammatory effects by reducing MPO, MDA, and TNF-alpha.