BACKGROUND: Eicosanoids are known to modulate inflammation. Moreover, some studies report that endogenous prostaglandin E(2) (PGE(2)) protects the pancreas against injury. Therefore, we investigated its role in a rat model of chronic alcohol consumption. METHODS: Rats were fed with 20% ethanol and a corn oil-supplemented diet using the interrupted alcohol feeding regimen (EI). Controls received water instead of ethanol (WI) or uninterruptedly ethanol (EU). After 13 mo, pancreas tissue was investigated morphologically, immunohistochemically and biochemically. RESULTS: Pancreatic tissue was more severely injured in EI than in WI and EU (p < 0.05). Fibrogenesis (alpha-smooth muscle actin-positive cells, collagen types I and III) was increased in EI compared to WI (p < 0.05). In EI, mast cell numbers were increased, compared to WI, but decreased, compared to EU (p < 0.05). EI showed decreased PGE(2) and malondialdehyde contents compared to EU (p < 0.05) and decreased glutathione concentrations compared to WI (p < 0.05). PGE(2) content and fibrogenesis were inversely correlated in EU. The same correlation was detectable as a trend in all alcohol-fed rats. CONCLUSION: The decrease in PGE(2) together with the increase in tissue damage and the inverse correlation between PGE(2) and fibrogenesis led us to suggest that endogenous PGE(2) plays a protective role in alcohol-induced injury in the pancreas. Copyright 2003 S. Karger AG, Basel and IAP
BACKGROUND:Eicosanoids are known to modulate inflammation. Moreover, some studies report that endogenous prostaglandin E(2) (PGE(2)) protects the pancreas against injury. Therefore, we investigated its role in a rat model of chronic alcohol consumption. METHODS:Rats were fed with 20% ethanol and a corn oil-supplemented diet using the interrupted alcohol feeding regimen (EI). Controls received water instead of ethanol (WI) or uninterruptedly ethanol (EU). After 13 mo, pancreas tissue was investigated morphologically, immunohistochemically and biochemically. RESULTS: Pancreatic tissue was more severely injured in EI than in WI and EU (p < 0.05). Fibrogenesis (alpha-smooth muscle actin-positive cells, collagen types I and III) was increased in EI compared to WI (p < 0.05). In EI, mast cell numbers were increased, compared to WI, but decreased, compared to EU (p < 0.05). EI showed decreased PGE(2) and malondialdehyde contents compared to EU (p < 0.05) and decreased glutathione concentrations compared to WI (p < 0.05). PGE(2) content and fibrogenesis were inversely correlated in EU. The same correlation was detectable as a trend in all alcohol-fed rats. CONCLUSION: The decrease in PGE(2) together with the increase in tissue damage and the inverse correlation between PGE(2) and fibrogenesis led us to suggest that endogenous PGE(2) plays a protective role in alcohol-induced injury in the pancreas. Copyright 2003 S. Karger AG, Basel and IAP