Background and purpose: Antiepileptic drugs  cause a wide range of side effects in patients, including hepatotoxicity particularly associated with valproic acid. In this study, the effects of administering the amino acid betaine in a model of liver damage caused by valproic acid in rats were investigated. Materials and methods: In this experimental study, 60 male Wistar rats weighing approximately 180 to 220 grams were used and divided into 6 groups. Liver damage was caused by administering 500 mg/kg of valproic acid for 14 consecutive days. Different doses of betaine, 10, 50, and 100 mg/kg, were administered VPA-treated rats. At the end of the intervention period, liver damage caused by valproic acid was assessed by examining serum biochemical parameters, including aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and bilirubin. The levels of reactive oxygen species (ROS), glutathione (GSH) reserves, total antioxidant ferric reducing antioxidant power (FRAP), and lipid peroxidation (LPO) were evaluated. Results: The results of this study showed that valproic acid (VPA) caused liver damage in rats, which was manifested as a significant increase in liver injury biomarkers such as ALT, AST, Bilirubin, and ALP. In the group that received only valproic acid, an increase in lipid peroxidation (LPO) and reactive oxygen species (ROS), along with a decrease in glutathione (GSH) reserves and total hepatic antioxidant capacity (FRAP), were observed. On the other hand, administration of betaine at different doses significantly reduced this liver damage. Conclusion: The findings of this study suggest that betaine can be potentially beneficial in the in the management or prevention of liver injury induced by valproic acid through the reduction of oxidative stress.caused by valproic acid and its consequences by reducing oxidative stress.