Non-alcoholic fatty liver disease (NAFLD) has become the most prevalent chronic liver disease globally, with its incidence rising annually. It can progress to cirrhosis and even hepatocellular carcinoma, posing a serious threat to human health. Stress can participate in the pathological process of NAFLD by activating inflammatory responses and regulating levels of inflammatory mediators, with hepatocyte injury being a core component of NAFLD progression. This paper focuses on three key stress-related inflammatory mediators: tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and C-reactive protein (CRP), elucidating their core mechanisms in the pathway related to stress signal, followed by inflammatory activation and hepatocyte injury respectively, and reviewing current research. Research indicates that certain inflammatory mediators can damage hepatocytes by directly inducing apoptosis or indirectly regulating metabolic disorders and fibrosis progression. However, questions regarding causal relationships, target specificity for intervention, and quantification of psychological stress remain unresolved. This paper aims to provide theoretical support for NAFLD intervention strategies targeting inflammatory mediators, clarifying future research directions to advance clinical translation.