Bisphenol A (BPA) has several potential uses, including in polycarbonate plastics and epoxy resins, which could expose humans to it. Recognized for its hepatotoxicity and ability to accumulate in organs. We prompted this study to explore the hepatoprotective potential of astaxanthin (ASTX), an antioxidant against BPA toxicity. We used 32 male Wistar Albino rats and randomly assigned them as: Control, Sham (olive oil), BPA, and BPA+ASTX. At the end of the experiment, Native Thiol, Total Thiol, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were measured in serum samples. Histopathological scoring was performed to evaluate the changes caused by ASTX in the liver. Caspase 3 and caspase 9 expression in liver tissues was demonstrated immunohistochemically and by PCR. Collagen I (COL1A1) and collagen III (COL3A1) mRNA levels were measured by PCR in the tissue samples. The BPA group showed elevated AST and ALT with decreased Thiol levels. ASTX administration reversed these changes as observed by reduced AST and ALT levels and increased Thiol levels. Histopathology indicated increased liver damage and fibrosis in the BPA group which were alleviated in the BPA+ASTX group. Gene expression analyses revealed upregulated COL1A1 and COL3A1 in BPA, which was downregulated with ASTX. Immunohistochemistry and PCR confirmed BPA-induced caspase 3 and caspase 9 expression, which were attenuated by ASTX. This study underscores ASTX's hepatoprotective efficacy against BPA-induced hepatotoxicity which ultimately attributed to its antioxidant and antiapoptotic properties. Consequently, ASTX emerges as a promising therapeutic agent for preventing and treating BPA-related liver diseases.