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

Saleem, Tahia; Abd EL-Aziz, Mohamed; El-Baz, Mona; Okda, Tarek; Abdel-Aziz, Hekmat

doi:10.21608/besps.2011.35959

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

Document Type : Original Article

Authors

¹ Department of Medical Biochemistry, Faculty of Medicine, Assuit Univrsity

² Department of Biochemistry, Faculty of pharmacy, Al-Azhar University (Assiut)

³ Department of Medical Biochemistry, Faculty of Medicine, Assuit Univrsity.

⁴ Department of Histology, Faculty of Medicine, Sohag university

10.21608/besps.2011.35959

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.