Abstract

Keeping in mind the beneficial effects of GTE administration on liver damage, the present study was undertaken to evaluate the hepatoprotective effect of green tea extract (GTE) against carbon tetrachloride (CCl4)-induced liver injuries in male hamsters for 8 weeks. Twenty hamsters were equally divided into 4 groups, the control ones (group I) received only dis. water. Hamsters of group II had free access to 10% of GTE, while hamsters of group III received 1ml/kg of 50% CCl4 in corn oil via gavage daily. Hamsters of group IV (GTE+CCl4) received a free access to GTE supplementation in combination with 1ml/kg of 50% CCl4 in corn oil via gavage daily. Lipid profile, hepatic enzyme levels and apoptosis molecular marker (p53) were investigated in hamsters. GTE+CCl4 treated hamsters showed lower levels of hepatic malondialdehyde (MDA) than CCl4 exposed hamsters. Hepatic activity levels of GSH, ALD and cytochrome 450 reductase were declined after CCl4 administration while they were remarkably improved with GTE administration. Serum lipid profiles as T-cholesterol (TC), triglyceride (TG) and low density lipoproteins (LDL) were improved in GTE and CCl4 treated hamsters than CCl4 group. Moreover, hepatic tissue damage and p53 expression induced with CCl4 were improved with the treatment of GTE. These results suggested that GTE possesses hepatoprotective properties against the effect of CCl4.

Highlights

  • CCl4 is a widely used industrial solvent and it is the bestcharacterized animal model of xenobiotic-induced, oxidative stress-mediated hepatotoxicity [36,25]

  • Oxygen-derived free radicals and lipid peroxidation play a critical role in the pathogenesis of various liver diseases including hepatic fibrosis [41,31], hepatic injury, apoptosis, and necrosis [56,29]

  • Green tea extract was tested in this study for its ameliorating effect to CCl4 induced hepatic injury in male hamsters through assessment of body weight, liver weight, lipid profile, MDA, GSH, LDH and cytochrome P450 reductase as well as p53 expression

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Summary

Introduction

CCl4 is a widely used industrial solvent and it is the bestcharacterized animal model of xenobiotic-induced, oxidative stress-mediated hepatotoxicity [36,25]. CCl4 induces the production of several types of reactive oxygen species (ROS), thereby causing liver injury [45]. These ROS can bind to polyunsaturated fatty acids, forming alkoxy and peroxyl radicals to produce lipid peroxide, causing cell membrane damage and changes in enzyme activity [52]. Oxygen-derived free radicals and lipid peroxidation play a critical role in the pathogenesis of various liver diseases including hepatic fibrosis [41,31], hepatic injury, apoptosis, and necrosis [56,29]. Elimination of free radicals and prevention of lipid peroxidation have been targeted in prevention and treatment of hepatic damage. Inhibiting p53-dependent hepatocyte apoptosis may be an effective therapeutic strategy for the treatment and prevention of hepatic fibrosis

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