Role of PGE2 in the Development of Pancreatic Injury Induced by Chronic Alcohol Feeding in Rats.

Autor: Siegmund, Eva, Weber, Heike, Kasper, Michael, Jonas, Ludwig
Zdroj: Pancreatology (Karger AG); 2003, Vol. 3 Issue 1, p26-35, 10p, 2 Diagrams, 4 Charts, 3 Graphs
Abstrakt: Background: Eicosanoids are known to modulate inflammation. Moreover, some studies report that endogenous prostaglandin E2 (PGE2) 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 (α-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 PGE2 and malondialdehyde contents compared to EU (p < 0.05) and decreased glutathione concentrations compared to WI (p < 0.05). PGE2 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 PGE2 together with the increase in tissue damage and the inverse correlation between PGE2 and fibrogenesis led us to suggest that endogenous PGE2 plays a protective role in alcohol-induced injury in the pancreas. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index
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