Galectin-3 in Repairing Damaged Mice Liver Induced By Ccl4: Role of Apoptosis and Oxidative Stress.

Abstract

Background: Carbon tetrachloride (CCl4) causes hepatic injury. Galectin-3 is amember of the lectin family; several studies have suggested that Gal-3 could repairliver damage. Objective: To estimate Gal-3 expressions in different periods after CCl4administration and to explore the mechanism of repair of the injured liver by Gal-3either through modulation of apoptosis or oxidative stress. Materials and methods:Twenty male mice (age 6 weeks; weight 25-30 g) were divided into 4 groups of 5 miceeach in separate cages with free access to food and water. Group (I): Control group.Groups II, III and IV administered orally CCl4 as a single dose 50% (W/W); CCl4 inolive oil at 2 ml/kg of body weight and left for 48, 72 and 96 hours respectively. Theperiod of repair of hepatocytes injured by CCl4 and signaling proteins intrinsic tothese periods were examined. Results: A 30 kDa polypeptide was detected by bothRT-PCR and Western blot analysis using anti-galectin-3 antibody in livers from mice48 to 96 hours after administration of a single dose of CCl4 and was identified asgalectin-3 in hepatocytes. Levels of Gal-3 were significantly higher in liver of mice at48 to 72 hour after CCl4 treatment compared to the control. Its level was reduced at96 hours after CCl4 administration. Bcl-2 levels increased significantly during theexperimental period after administration of CCl4, where presented in low amount inthe control mice. Caspase-3 was detected in trace amount in control mice, increasedafter 48 and 72 hours from administration of CCl4 and then decreased gradually at96 hours. Both tissue homogenate levels of nitric oxide and lipid peroxidation showedmarked increase at 48 hours as compared to controls. Their levels decreasedgradually at 72 and 96 hours after CCl4 administration. The tissue homogenate levelsof antioxidants CAT, GSH and SOD activity of all groups were significantlydecreased at 48 hours and then increased gradually at 72 and 96 hours after CCl4administration but did not reach to normal level. Conclusion: Gal-3 plays animportant role in repairing the hepatocellular damage which occurred by CCl4through its role as anti-apoptotic agent and against free radical generation.