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Ischemia-reperfusion (IR) injury constitutes the most important cause of primary dysfunction of liver grafts. In this study, we have addressed the possible hepatoprotective action of liraglutide against partial warm hepatic IR injury in male rats. Rats were randomly assigned into: sham, IR, and liraglutide-pretreated IR groups. Liraglutide was administered 50 μg/kg s.c. twice daily for 14 days, and then, hepatic IR was induced by clamping portal vein and hepatic artery to left and median lobes for 30 min followed by reperfusion for 24 h. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma glutamyl transferase (GGT) activities were determined. Malondialdehyde (MDA) level, reduced glutathione (GSH) content, tumor necrosis factor-α (TNF-α), phosphoralated Akt (p-Akt), and caspase-3 levels of the liver were determined. Hematoxylin and eosin (H&E) stained sections from liver were examined as well as immunohistochemical sections for detection of Bcl-2 expression. IR injury increased ALT, AST, and GGT while decreased GSH and p-Akt with increase in MDA, TNF-α, and caspase-3 levels in the liver with necrosis and inflammatory cellular infiltration with decreased Bcl-2 expression. Pretreatment with liraglutide decreased ALT, AST, and GGT activities while increased glutathione content and Akt activation with decrements in MDA, TNF-α, and caspase-3 levels with attenuation of necrosis and inflammation while enhanced Bcl-2 expression in the liver. Liraglutide protects against IR injury of the liver through antiinflammatory and antioxidant actions as well as inhibition of apoptosis.

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Background: Liver injuries induced by various hepatotoxins have been recognized as a major toxicological problem for years. 3-Hydroxy-3-methyglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) are widely used drugs to reduce cholesterol levels and prevent coronary heart disease. One of the adverse effects of statins is affection of the liver functions with increased transaminases levels. Propolis is collected by honeybees from various plant sources. It was found to have hepatoprotective activity. Aim: The present study evaluated the possible hepatoprotective effect of propolis against hepatotoxic effect of atorvastatin in albino rats. Methods: Propolis in doses of 50 and 100mg/kg were administered one hour before atorvastatin in doses of 20 and 80mg/kg daily, orally for one month. Hepatoprotective effect of propolis was evaluated by measuring levels of ALT and AST in the serum and SOD and CAT in the liver homogenate. The histopathological studies were also studied to support the biochemical parameters. Results: Atorvastatin in a dose of 20 and 80mg/kg produced dose-dependent, significant elevation of ALT, AST, SOD, CAT and hepatocyte degeneration. Administration of propolis 50 and 100mg/kg produced dose-dependent, significant reduction of the previous biochemical parameters and also prevented atorvastatin induced alterations in histoarcheticture of liver in a dose dependent manner. Conclusion: Propolis protected the liver from the toxic effect of atorvastatin. The hepatoprotective effect of propolis may be due to its strong antioxidant activity.

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