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.