الفهرس 
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Abstract
Our current study was conducted on 60 normal adult male albino rats that were handled carefully and divided into six groups as follows after 2 weeks of acclimatization: the first group served as control, the second group (TAA) administered IP injection of TAA at 100 mg/kg BW every other day, the third group (VD) administered IM injection of Devarol S 200000 at 1000 IU/kg BW day by day, the fourth group (TAA+VD) dual treatment was administered the same doses of TAA and VD3, the fifth group (Hesp) treated orally at a dose of 200 mg/kg BW daily and the last group dual treatment were administered the same doses of TAA and Hesp. At the end of the eighth week of our research, blood samples were collected from the retro-orbital plexus: The first sample was collected in Eppendorf tubes containing K3EDTA and well mixed for a complete blood picture, The second one was collected in plane tubes and then centrifuged at 1500 rpm for 10 min and sera were collected and chilled at -20°C in Eppendorf tubes for serum biochemical analysis. Consequently, the rats were sacrificed in compliance with the institutional policies of the Faculty of Veterinary Medicine’s Animal Research Ethical Committee at Mansoura University in Egypt (Ph.D/46) by cervical dislocation. Liver tissues were divided into 3 pieces: the first part, weighing 0.5 g for evaluation of liver oxidative and antioxidant biomarkers; the second portion for gene expression analysis; and the last portion was fixed in 10% neutral buffered formalin and prepared for H&E and Masson’s trichrome staining of liver architecture and assessment of fibrosis scoring, in addition to immunohistochemical examination. from this study, it was concluded that: Oxidative stress, inflammation, and apoptosis play an important role in TAA-induced hepatotoxicity. The treatment with VD3 and Hesp acts as a hepatoprotective agent against TAA-induced hepatotoxicity and fibrosis with the best results for VD3 which were confirmed by histopathology.