We used an animal model of chronic alcohol-induced liver injury that is associated with increased intestinal permeability. Male Wistar rats were given increasing alcohol doses from 2 g/kg/d to 8 g/kg/d and alcohol plus PRE via intragastric feeding for 10 weeks. Chronic alcohol exposure caused an elevation in serum alanine aminotransferase (ALT) as well as aspartate aminotransferase (AST) levels and a decrease in superoxide dismutase (SOD) activity, and hepatic damages including steatosis, inflammation, and necrosis, determined by serum enzymatic analysis and morphological analysis, respectively. The damage to small intestine induced by chronic alcohol treatment was examined by intestinal histological, immunohistochemical analysis, and permeability assays.
Alcohol-induced hepatic pathological changes, elevations in ALT and AST, and a decrease in SOD activity were significantly inhibited in PRE treated animals. The inhibitory effect of PRE on alcohol-induced liver injury was associated with suppression of alcohol induced the increase of intestinal permeability.
The results showed that this beneficial effect of PRE on ALD could be partly explained by improving intestinal barrier dysfunction induced by alcohol.