Possible Effect of Mosapride on Gastric Mucosa and Indomethacin Induced Gastric Ulcer in Male Albino Rats

Sohair S El Menshawy,Laila R,Amira A,Gehane A El-Gindy,Amira M Abd Elhamid,Ahmed A Abd El-Sameea

doi:10.11131/2014/101349

Abstract

Possible Effect of Mosapride on Gastric Mucosa and Indomethacin Induced Gastric Ulcer in Male Albino Rats

Highlights

Acute liver failure (ALF) is a devastating clinical syndrome characterized by abrupt onset of severe acute liver injury, occurring in a patient with no preexistent liver disease, causing multi organ failure with extremely high mortality rates (Fix, 2013)
The present study aimed to investigate the possible mechanisms underlying the hepatoprotective effect of Vanillic acid (VA) on TAA- induced ALF in rats, by studying its effect on several oxidative stress and anti-inflammatory markers, and whether it could ameliorate the progression of the disease
The protection effect of VA was acting in a dose dependent manner significantly in the level of ALT and total bilirubin level (TB) only

Summary

Introduction

Acute liver failure (ALF) is a devastating clinical syndrome characterized by abrupt onset of severe acute liver injury, occurring in a patient with no preexistent liver disease, causing multi organ failure with extremely high mortality rates (Fix, 2013). Liver transplantation remains the only curative treatment option. This treatment option is limited by scarcity of donor organs, lifelong immunosuppressant and high costs (Morabito and Adebayo, 2014). Excessive oxidative stress and inflammation are well established to play a central role in the pathogenesis of ALF regarding the initiation and the progression of the disease. They are inextricably linked as one begins the other is amplified, and they work together to aggravate liver injury (Jaeschke and Ramachandran, 2011; Zimmermann et al, 2012). Reactive oxygen species (ROS) cause tissue injury directly by affecting tissue lipids, proteins and DNA as well as indirectly by triggering inflammation, leucocytes accumulation in liver tissue with massive release of inflammatory mediators that induce further ROS liberation, amplifying the inflammatory response and exacerbating liver tissue damage (Jaeschke, 2011; Bosoi and Rose, 2013)

Methods

Results

Conclusion