AMELIORATIVE POTENTIAL OF GREEN TEA AND OMEGA-3 AGAINST ALUMINIUM CHLORIDE-INDUCED HEPATOTOXICITY IN RABBITS

Abstract

Background: Aluminium chloride has been reported to cause toxic effects on the liver by triggering oxidative stress, damaging hepatocytes, and impairing normal hepatic functions. Some natural antioxidants, like green tea and omega-3 fatty acids, can stop such toxic effect, because of their superior anti-inflammatory and free radical scavenging capabilities. The purpose of the current study was to determine whether green tea and omega-3 fatty acids could reduce the hepatotoxicity caused by AlCl₃ in rabbits. Methods: 32 mature rabbits were homogeneously divided into four groups (n = 8). Group I (control group) was given regular diet and distilled water. Group II received AlCl₃ (300 mg/kg) orally, one time in a day for 30 days. Group III was orally given AlCl₃ (300 mg/kg) with green tea extract (50 mg/kg/day), while Group IV was orally given AlCl₃ (300 mg/kg) with omega-3 fatty acids (20 mg/kg/day). Body weight measurement at regular intervals, liver function tests (ALT, ALP, and total bilirubin level), and histopathology were studied. Results: Aluminium chloride led to decrease in weight, while green tea and omega-3 supplementation preserved body weight closer to control values. Aluminium chloride greatly increased RLW when compared with control values, while green tea and omega-3 co-supplementation greatly reduced RLW to near normal values. AlCl₃ greatly elevated ALT, ALP, and total bilirubin values, while both treatments greatly reduced these parameters to near normal values with respect to their efficacy with omega-3 reporting maximum activity. By Histopathological analysis, hepatocellular necrosis, inflammation, and fibrosis were observed in AlCl₃ group. Conclusion: Green tea or omega-3 supplementation greatly rehabilitated biochemical parameters with improved histological architecture. These hepatoprotections can be attributed to green tea and omega-3's antioxidant and anti-inflammatory activities, thereby they potently act as natutal antioxidants (NATs) for chemically induced liver damages.