Effects of Anti-ulcer Agents on Ethanol-induced Gastric Mucosal Lesions in D-Galactosamine-induced Hepatitis Rats

Abstract

Patients with hepatic injury have an increased incidence of gastric ulcers and erosions. In this study, the effect of D-galactosamine(GalN)-induced hepatitis on ethanol-induced gastric mucosal lesions and the protective effect of anti-ulcer agents in rats were examined. Subcutaneous injection of GalN (1 g/kg) remarkably increased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities suggesting induction of hepatic injury. Gastric mucosal lesions induced by ethanol were significantly aggravated in GalN-induced hepatitis rats. Orally administered ecabet (CAS 86408-72-2; 20-200 mg/kg) dose dependently inhibited ethanol-induced gastric mucosal lesions in GalN-induced hepatitis rats. Sucralfate (CAS 54182-58-0) tended to inhibit the gastric mucosal lesions at a dose of 200 mg/kg but teprenone (CAS 6809-52-5), cimetidine (CAS 51481-61-9) and rebamipide (CAS 90098-04-7) had little effect. All anti-ulcer agents had no effect on the serum ALT and AST activities increased by GalN pretreatment. These results indicate that the gastric mucosa of GalN-induced hepatitis rats is more susceptible to injury induced by luminal irritants such as ethanol. Ecabet potently inhibited gastric mucosal lesions suggesting its clinical utility for the gastric mucosal damage in patients with hepatic injury.

Inhibition of 5-Lipoxygenase Pathway Attenuates Acute Liver Failure by Inhibiting Macrophage Activation

“…Peritoneal injection of D-GalN with LPS induces liver damage that closely resembles human viral hepatitis [20–22]. Thus, we chose to use this method to construct a rat model to imitate ALF caused by viral hepatitis in humans.…”

Protective effect of low molecular fraction of MGN-3, a modified arabinoxylan from rice bran, on acute liver injury by inhibition of NF-κB and JNK/MAPK expression

“…GalN is used as an experimental model of severe hepatic damage that closely resembles human viral hepatitis, due to its ability to inhibit RNA and protein synthesis in the liver, resulting in the subsequent release of endotoxin from the intestine [5,[26][27][28]. Endogenously produced endotoxin has been implicated as a cofactor in GalN-induced hepatocellular injury, death [29,30] and TNF hypersensitivity [31].…”

Hypolipidemic action of chrysin on Triton WR-1339-induced hyperlipidemia in female C57BL/6 mice

“…The liver is a key organ for lipid metabolism since hepatic cholesterol uptake from serum, coupled with intracellular processing and biliary excretion is an important feature in removal of excess cholesterol from the body, beyond synthesis and metabolism of cholesterol, bile acids and phospholipids [1] . Cholesterol is an essential constituent of most biological membranes, besides acting as a precursor for the synthesis of bile acids, hormones and vitamins [2] .…”