Non-alcoholic fatty liver disease (NAFLD) is currently the most prevalent chronic liver disease worldwide, posing a significant threat to human health; however, its pathogenesis remains incompletely understood. Research on regulatory cell death has opened new avenues for disease treatment. Among these, ferroptosis is a form of iron-dependent non-apoptotic cell death, which can be triggered by disturbances in iron metabolism, oxidative stress, and the accumulation of lipid peroxides. Given the liver's critical role in iron storage and lipid metabolism, recent studies have established a close association between ferroptosis and NAFLD. Abnormal lipid accumulation within cells can lead to redox imbalance, which may be a key factor contributing to lipid metabolism disorders. Consequently, inhibiting ferroptosis has emerged as a potential therapeutic strategy for NAFLD. Glutathione peroxidase 4 (GPX4) is a pivotal regulatory protein in ferroptosis, capable of binding to reduced glutathione (GSH) to degrade reactive oxygen species (ROS) and hydrogen peroxide (H2O2), thereby mitigating lipid peroxidation damage. Current research indicates that active components from traditional Chinese medicines, such as Astragalus, green tea, and Coptis, can modulate GPX4 through multiple targets, thereby influencing NAFLD. This review explores the mechanisms by which GPX4 operates within the ferroptosis pathway and identifies herbal extracts that may offer therapeutic benefits for NAFLD through GPX4 regulation.