Galectin-3 in Repairing Damaged Mice Liver Induced By Ccl4: Role of Apoptosis and Oxidative Stress. | ||||
| Bulletin of Egyptian Society for Physiological Sciences | ||||
| Article 3, Volume 31, Issue 1, December 2011, Page 29-42 PDF (688.56 K) | ||||
| Document Type: Original Article | ||||
| DOI: 10.21608/besps.2011.35959 | ||||
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| Authors | ||||
| Tahia Saleem* 1; Mohamed Abd EL-Aziz2; Mona El-Baz3; Tarek Okda2; Hekmat Abdel-Aziz4 | ||||
| 1Department of Medical Biochemistry, Faculty of Medicine, Assuit Univrsity | ||||
| 2Department of Biochemistry, Faculty of pharmacy, Al-Azhar University (Assiut) | ||||
| 3Department of Medical Biochemistry, Faculty of Medicine, Assuit Univrsity. | ||||
| 4Department of Histology, Faculty of Medicine, Sohag university | ||||
| Abstract | ||||
| Background: Carbon tetrachloride (CCl4) causes hepatic injury. Galectin-3 is a member of the lectin family; several studies have suggested that Gal-3 could repair liver damage. Objective: To estimate Gal-3 expressions in different periods after CCl4 administration and to explore the mechanism of repair of the injured liver by Gal-3 either 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 mice each 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 in olive oil at 2 ml/kg of body weight and left for 48, 72 and 96 hours respectively. The period of repair of hepatocytes injured by CCl4 and signaling proteins intrinsic to these periods were examined. Results: A 30 kDa polypeptide was detected by both RT-PCR and Western blot analysis using anti-galectin-3 antibody in livers from mice 48 to 96 hours after administration of a single dose of CCl4 and was identified as galectin-3 in hepatocytes. Levels of Gal-3 were significantly higher in liver of mice at 48 to 72 hour after CCl4 treatment compared to the control. Its level was reduced at 96 hours after CCl4 administration. Bcl-2 levels increased significantly during the experimental period after administration of CCl4, where presented in low amount in the control mice. Caspase-3 was detected in trace amount in control mice, increased after 48 and 72 hours from administration of CCl4 and then decreased gradually at 96 hours. Both tissue homogenate levels of nitric oxide and lipid peroxidation showed marked increase at 48 hours as compared to controls. Their levels decreased gradually at 72 and 96 hours after CCl4 administration. The tissue homogenate levels of antioxidants CAT, GSH and SOD activity of all groups were significantly decreased at 48 hours and then increased gradually at 72 and 96 hours after CCl4 administration but did not reach to normal level. Conclusion: Gal-3 plays an important role in repairing the hepatocellular damage which occurred by CCl4 through its role as anti-apoptotic agent and against free radical generation. | ||||
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