As is widely recognized, exercise can effectively prevent and alleviate non-alcoholic fatty liver disease (NAFLD), but its mechanism remains to be further explored. In recent years, studies have revealed that the polarization of liver macrophages is closely associated with NAFLD. Based on a review of the characteristics of macrophage polarization at each stage of NAFLD, this article further analyzes the influence of exercise on macrophage polarization and its therapeutic efficacy for NAFLD. The results indicate that under normal circumstances, the resident Kupffer macrophages in the liver maintain a dynamic banlance between the pro-inflammatory M1 and anti-inflammatory M2 phenotypes. In the early stage of NAFLD, aerobic exercises of different intensities can suppress the increase of M1/M2 ratio and exert remarkable effects on the early stage of NAFLD by inhibiting the infiltration of exogenous macrophages or the polarization of Kupffer cells towards the M1 phenotype. With the further development of NAFLD, liver macrophages gradually exhibited an increased phenomenon of stress-induced M2 polarization. However, at this juncture, the principal role of M2 macrophages is manifested in facilitating the activation of hepatic stellate cells and the differentiation of the extracellular matrix, thereby inducing liver fibrosis and even cirrhosis or liver cancer. In summary, this study suggests that macrophage polarization may be a new target for exercise to prevent NAFLD. Blocking the infiltration of exogenous macrophages or inhibiting the M1 polarization of Kupffer cells may be an important strategy to prevent the progression of NAFLD. However, when the disease progresses to the stage of fibrosis, cirrhosis, or liver cancer, avoiding the stress-induced M2 polarization of macrophages may be an effective therapeutic target.

运动防治非酒精性脂肪性肝病（NAFLD）的效果已被普遍认可，但对其机制的研究一直未有突破性进展。肝脏巨噬细胞极化状态与NAFLD的发生、发展关系密切，但研究成果缺乏有效的整合。本文在解析肝脏巨噬细胞极化与NAFLD各阶段关系的基础上进一步分析运动对巨噬细胞极化的影响及其对NAFLD的治疗效果。结果表明，正常情况下肝脏常驻库普弗巨噬细胞维持促炎M1和抗炎M2表型间的动态平衡；在NAFLD早期阶段，不同强度的有氧运动均可通过抑制外源巨噬细胞浸润或抑制库普弗细胞向M1型极化，进而抑制M1/M2比值升高，对NAFLD早期防治效果显著；此后肝脏巨噬细胞逐渐出现应激性M2型极化增加现象，但此时其主要作用表现为促进肝星状细胞的激活和细胞外基质的分化，导致肝纤维化甚至肝硬化和肝癌。综上，本研究提示，巨噬细胞极化可能是运动防治NAFLD的新靶向，阻滞外源巨噬细胞浸润或抑制库普弗细胞向M1型极化是预防NAFLD进展的重要策略；而当疾病发展为纤维化、肝硬化或肝癌阶段，避免巨噬细胞向M2型的应激性极化可能是有效的治疗靶向。