Pentoxifylline contributes to the hepatic cytoprotective process in rats undergoing hepatic ischemia and reperfusion injury

Aim: Considerable efforts have been made to find and/or eliminate the under yling causes of hepatic ischemia-reperfusion injury, but many points are st ill unclear. Pentoxifylline-related cytoprotection is one of these unclear points. Our study tests the effects of pentoxifylline on the hepatic cytopr otective process in an experimental model. Materials and Methods: The anima ls were divided into two groups: (1) placebo-pretreated rats and (2) pentox ifylline-pretreated rats. After pretreatment, all rats underwent the hepati c ischemia-reperfusion procedure which was performed by clamping the hepato duodenal ligament. To evaluate the liver injury, serum levels of alanine tr ansaminase (ALT) and aspartate transaminase (AST), and liver tissue levels of prostaglandin E-2 (PGE(2)) were measured before ischemia, immediately af ter ischemia and immediately after reperfusion. Results: Before ischemia an d immediately after ischemia, there were no significant differences between ALT and AST levels of groups 1 and 2 (p >0.05). However, at the end of rep erfusion, ALT and AST levels of group 2 were significantly decreased when c ompared with group 1 (p < 0.05 and p < 0.01, respectively). Additionally, t issue levels of PGE2 that were obtained before ischemia, immediately after ischemia and immediately after reperfusion in group 2 were significantly hi gher than those of group 1 (p < 0.001). Conclusion: Pentoxifylline reduces reperfusion injury of the liver through significantly decreased transaminas e levels, and contributes to hepatic cytoprotection by increasing tissue le vels of PGE2 significantly. These effects reflect the role of tissue PGE2 i n pentoxifylline-related hepatoprotection against ischemia-reperfusion inju ry of the liver.