Background: Hepatotoxicity is the term used to describe harm or liver damage brought on by drug use or other nonpharmacological factors. White crystal chemical acrylamide (ACR) is a typical raw material for polyacrylamide products. Traditional Chinese medicine called Effect of Ginkgo Biloba (EGb) comprises flavonoids and other active ingredients with significant medicinal qualities. Administration of EGb repaired the harm caused by ACR. The protective effect of EGb is achieved by encouraging neuronal regeneration. It is commonly known that EGb works very well to increase antioxidants and blood flow to the brain. Objectives: The aim of the current work was to assess by histological and biochemical tests the potential protective impact of Ginkgo biloba extract against the hepatotoxicity caused by acrylamide. Materials and methods: Forty Wister male albino rats of the local strain of average body weight 160±15 g were used in this study. The experimental healthy animals were housed in separate appropriate cages with a 12-hour light/dark cycle in an environmentally controlled breeding room at a temperature of 22°C and a humidity of 60%, with free access to food and water. Rats were fed a standard diet of processed rat food and water. Liver enzymes and Oxidative stress indicators were measured. Results: Alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase levels were significantly higher in the acrylamide-treated group compared to the untreated, ginkgo biloba-treated, and acrylamide + ginkgo biloba-treated groups (P<0.001). Malondialdehyde levels were also considerably higher in the acrylamide-treated group (20.021.91) compared to the untreated control group (5.220.66), the ginkgo biloba-treated group (4.590.35), and the acrylamide + ginkgo biloba-treated group (8.411.24) (P<0.001). Conclusion:It could be concluded that the hepatoprotective of Ginkgo Biloba action serves as a preventative and therapeutic measure. An aqueous extract of G. biloba leaf contains a variety of chemical components that may function as a mechanism to reduce acute liver damage by scavenging oxidative free radicals, inhibiting lipid peroxidation, and possessing antioxidant activity.

Background: Liver fibrosis is one of the main complications of chronic liver disease and is the main reason for increased mortality in affected patients. Fibrosis is characterized by excess deposition of extracellular matrix components including different collagens and non-collagenous proteins such as laminin, fibronectin and undulin.Objective: This study aimed to: (1) Evaluate the possible hepatoprotective effect of nebivolol and carvidelol on carbon tetrachloride (CCl4)-induced liver fibrosis. (2) Compare between hepatoprotective effect of nebivolol and carvidelol on CCl4-induced liver fibrosis on normotensive and hypertensive rats. Materials and Methods: This study was conducted on 110 male albino rats. Animals were obtained from the animal house of Faculty of Medicine, Assiut University. Their weight ranged between 160-200 grams each at the beginning of the experiment. Rats were housed in 11 groups with 10 rats each in clean capacious macrolane cages under standard laboratory conditions including good aerated room with suitable temperature (25 ± 5°C) and maintained at good light. Standard rodent food and water were available ad libitium. Results: Subcutaneous injection of CCl4 for 8 weeks caused hepatic pathological damage and significantly increased the levels of serum AST, ALT, ALP, hepatic malondialdehyde and hydroxyproline content. Moreover, it decreased the activities of superoxide dismutase and glutathione. Treatment with silymarin, carvedilol and nebivolol decreased significantly the AST, ALT, and ALP levels in plasma, MDA and hydroxyproline in liver tissues, and increased the activities of SOD and glutathione in liver tissue. Conclusion:The biochemical and histopathological changes induced by administration of CCl4 were improved under the effect of the used drugs in variable degrees. The most efficient drug was silymarin followed by carvedilol then nebivolol.