Khattab, H. (2012). Effect of Ginkgo biloba Leaves Aqueous Extract on Carbon Tetrachloride Induced Acute hepatotoxicity in rats. The Egyptian Journal of Hospital Medicine, 48(1), 483-495. doi: 10.21608/ejhm.2012.16250
Hala A.H. Khattab. "Effect of Ginkgo biloba Leaves Aqueous Extract on Carbon Tetrachloride Induced Acute hepatotoxicity in rats". The Egyptian Journal of Hospital Medicine, 48, 1, 2012, 483-495. doi: 10.21608/ejhm.2012.16250
Khattab, H. (2012). 'Effect of Ginkgo biloba Leaves Aqueous Extract on Carbon Tetrachloride Induced Acute hepatotoxicity in rats', The Egyptian Journal of Hospital Medicine, 48(1), pp. 483-495. doi: 10.21608/ejhm.2012.16250
Khattab, H. Effect of Ginkgo biloba Leaves Aqueous Extract on Carbon Tetrachloride Induced Acute hepatotoxicity in rats. The Egyptian Journal of Hospital Medicine, 2012; 48(1): 483-495. doi: 10.21608/ejhm.2012.16250
Effect of Ginkgo biloba Leaves Aqueous Extract on Carbon Tetrachloride Induced Acute hepatotoxicity in rats
Nutrition and Food Science Dept., Faculty of Home Economics, Helwan University
Abstract
Bachground: Oxidative stress plays a pivotal role in the pathogenesis and progression of various liver diseases. Ginkgo biloba leaves extract (GbE) have been proved to be an effective antioxidant, thereby can contribute to the prevention and treatment of diseases associated with oxidative stress.The present study aimed to investigate the hepatoprotective effect of GbE on acute liver injury induced using carbon tetrachloride (CCl4) in rats. Material and Methods: Hepatotoxicity was induced in male rats by intraperitoneal (i.p) injection of CCl4 1mL/ kg body weight (b.w.) for every 72 h for 14 days, GbE was administered orally at a dose of 150 mg/kg b.w., daily started two weeks prior to CCl4 injection and continued until the end of the experiment. Results: CCl4 caused acute liver damage in rats, as evidenced by significant increase serum enzymes activities of aspartate and alanine aminotransferase (ALT & AST) and alkaline phosphatase (ALP), and hepatic malondialdehyde (MDA), as well as significant decrease in weight gain percent, serum total protein (TP), high-density lipoprotein cholesterol (HDL-C), and hepatic reduced glutathione (GSH). Pretreatment with GbE prior to CCl4 injection elicited hepatoprotetcive activity by significant decreased the activities of liver enzymes and hepatic MDA, and significant increased the levels of TP, and hepatic GSH, as well as induced significant ameliorated in weight gain percent and lipid profileparameters as compared with CCl4 group. Histopathological examination of the liver tissues of CCl4 group represented the presence of hepatic necrosis associated with cells infiltration and vacuolar degeneration of hepatocytes, while the pretreatment with GbE overcome these changes, the majority of the cells tend to be normal. Conclusion: The present findings indicated that the hepatoprotective effect of GbE against CCl4-induced oxidative damage may be due to its potent antioxidant activity. Therefore, GbE could be of potential help as a medicament or food supplement for alleviation of liver toxicity.
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