Antioxidative effect of prostaglandin E2 in thioacetamide-induced liver cirrhosis.

Several studies provided evidence that various prostaglandins exhibited a hepatoprotective effect in vivo as well in vitro the mechanism of which is still in debate. Therefore, the aim of our studies was to examine the effect of PGE2 on some biochemical and morphological alterations in chemically induced liver cirrhosis in rats. A micronodular liver cirrhosis was induced by treatment of rats with thioacetamide for 3 months. Morphologically, the administration of PGE2 for 8 days reduced the extent of vacuolar transformation of the hepatocytes and the density of the nuclear structure without affecting the fibrotic state as assessed by the hepatic hydroxyproline content. The widening of the sinusoids indicated an improved hepatic microcirculation. Administration of PGE2 significantly elevated the percentage portion of arachidonic (20:4) and docosapentaenoic (22:5) acid in the hepatic phospholipids and reduced the ratio 20:3/20:4 fatty acids in comparison to the untreated cirrhotic animals. The hepatic MDA concentration was decreased by 40% in PGE2-treated animals. PGE2 treatment also reduced the content of polar as well as of non-polar carbonyls when compared with the controls. Moreover, treatment with PGE2 lowered iron-induced or iron plus ascorbate-induced MDA production of isolated hepatocytes. From the data it was concluded that the hepatoprotective effect of PGE2 may be related to its antioxidative capacity.