Oxidative stress has an important role in determining severe damage to the liver, including steatosis. Curcumin (CUR) is a natural polyphenol compound with antioxidant potential but its mechanism is still unclear. In this study, 2% ethanol (ETH) was used to establish a liver injury model in Tg (fabp10: Ps Red) transgenic zebrafish with the fluorescent liver. Ethanol-treated zebrafish had an increased vacuole rate at 144 h post-fertilization (hpf), thus confirming the effectiveness of the proposed model in inducing liver damage. However, when ethanol was submitted to co-exposure with curcumin, fluorescence area and signal intensity, as well as vacuole rate, were similar to the levels found in the control group. RNA-seq results showed that ethanol and CUR affected the regulation of catalytic activity and phenylalanine metabolism, biosynthesis of amino acids, and arginine and proline metabolism signaling pathways. QRT-PCR analysis also showed that treatment with CUR led to the downregulation of genes involved in the Nrf2-Keap1 signaling pathway and altered the expression pattern of genes related to glutathione metabolism (gsr, gpx1a, gstp1, gsto1, and idh1a). CUR also induced an increase in GSH content and recovered decreased GSH caused by ethanol exposure. The findings discussed herein indicate that CUR can promote glutathione synthesis, which aided in the recovery from ethanol-induced liver damage in zebrafish larvae.