الفهرس 
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Abstract
Introduction: The liver is a crucial organ for the maintenance of homeostasis and body functions in general. Its optimal function, therefore, is crucial for health and disease. It is the principal site for metabolism, excretion and detoxifier of unwanted substances. It is the principal site for metabolism, excretion and detoxifier of unwanted substances. Hepatotoxicity can produced due to medicines, chemicals, dietary disturbances or even herb. Experimentally, a variety of drugs and chemicals are used to induce animal model of hepatotoxicity.Aim of the work: The present study was conducted to explore the beneficial effect of date palm fruit extract (DPFE), which possesses antioxidant and hepatoprotective activity, on CCl4 or DENA- induced hepatic toxicity in adult male rats.Materials and Methods: This study was performed on thirty six adult male Wister albino rats, weighing ~ 140 g. After two week of acclimatization, the male rats were randomly divided into six groups. CCl4 and DENA were given in a single intraperitoneal (ip) dose of 3ml/kg and 150 mg/kg, respectively. Also DPFE was taken in a dose of 1g/kg.Results: Rats injected with CCl4 or DENA showed significant increases in the serum levels of ALT, AST, ALP, TB; and significant decrease in TP and ALB. Moreover, there were significant elevations in the hepatic content of MDA; and a significant inhibition in both the level of GSH and the activities of antioxidant enzymes including SOD, CAT, GPx and GST in the liver of the intoxicated rats. On the other hand, the results exhibited marked enhancement in the concentrations of TL, TC, TG and LDL-C; while the level of HDL-C was significantly decreased in CCl4- or DENA-treated rats. Pretreatment with DPFE (1g/kg) for 4 weeks to rats injected with a single dose of either CCl4 (3ml/kg) or DENA (150 mg/kg) significantly alleviated the toxin-induced detrimental effects in the above mentioned biochemical parameters. Conclusion: Long-term pretreatment with DPFE showed prophylactic effect against either CCl4- or DENA-induced hepatotoxicity, as manifested by reducing the deleterious changes in the markers of liver function, oxidative stress and lipid profile in the treated rats. The hepatoprotective effect of DPFE against liver injury induced by either CCl4 or DENA could be attributed to its biological components that possess antioxidant activity and free radicals scavenging ability.