目的 探究祛湿活血方对游离脂肪酸（FFA）诱导的HepG2细胞的作用及机制。 方法 采用体外细胞实验，利用CCK8法测定不同浓度祛湿活血方对HepG2细胞活性的影响以选定适宜浓度进行后续实验。随后使用250 μmol/L棕榈酸钠溶液联合500 μmol/L油酸钠的游离脂肪酸处理24 h诱导建立脂肪肝细胞模型，并给予不同浓度祛湿活血方含药血清及AMPK抑制剂对HepG2细胞进行24 h干预。通过油红O染色法和脂质荧光染色法观察细胞内脂滴积聚情况，采用GPO-PAP酶法检测细胞内总胆固醇（TC）和甘油三酯（TG）含量变化，TBA法检测和羟胺法分别检测丙二醛（MDA）和超氧化物歧化酶（SOD）的含量，ELISA检测肿瘤坏死因子-α（TNF-α）和白细胞介素1β（IL-1β）的含量，进一步运用qRT-PCR、Western blot和免疫荧光染色技术检测细胞内脂质代谢相关基因及蛋白的表达。 结果 祛湿活血方可显著改善FFA诱导的HepG2细胞脂质沉积，氧化应激及炎症反应，显著降低细胞中TC、TG、MDA、TNF-α、IL-1β的含量和提高SOD活性（P < 0.01），提高AMPK，降低SREBP1c、FASN、ACC1和SCD1的mRNA表达水平（P < 0.05），以及增加p-AMPK/AMPK，降低SREBP1c、FASN、ACC1和SCD1的蛋白表达（P<0.05）。 结论 祛湿活血方能够显著改善MASLD细胞模型的脂质代谢，并减轻氧化应激及炎症反应，其机制可能与激活AMPK/SREBP1c信号通路有关。

Objective To investigate the effect of Qushi Huoxue decoction （QSHXF） on free fatty acid （FFA）-induced HepG2 cells and its underlying mechanism. Methods In vitro cell experiments were conducted. First， the CCK-8 assay was used to determine the effects of different concentrations of QSHXF on HepG2 cells viability to select appropriate concentrations for subsequent experiments. A fatty liver cell model was then established by treating HepG2 cells with a mixture of 250 μmol/L sodium palmitate and 500 μmol/L sodium oleate for 24 h， followed by intervention with different concentrations of QSHXF-containing serum and AMPK inhibitor for another 24 h. Intracellular lipid droplet accumulation was observed using Oil Red O staining and lipid fluorescence staining. The levels of total cholesterol （TC） and triglycerides （TG） were measured using the GPO-PAP enzymatic method. The TBA method and hydroxylamine method were used to detect malondialdehyde （MDA） and superoxide dismutase （SOD）， respectively， while ELISA was used to detect tumor necrosis factor-α （TNF-α） and interleukin 1β （IL-1β）. Furthermore， qRT-PCR， Western blot， and immunofluorescence staining were performed to detect the expression of lipid metabolism-related genes and proteins. Results QSHXF significantly improved the lipid deposition， oxidative stress and inflammatory response of FFA-induced HepG2 cells， markedly reduce the content of TC， TG， MDA， TNF-α and IL-1β in cells and increase the activity of SOD （P < 0.01）. Meanwhile， it increased the mRNA expression of AMPK and the protein ratio of p-AMPK/AMPK， while decreasing the mRNA and protein levels of SREBP1c， FASN， ACC1， and SCD1 （all P < 0.05）. Conclusion QSHXF significantly improved lipid metabolism and alleviated oxidative stress and inflammation in the MASLD cell model， and its mechanism may be associated with the activation of the AMPK/SREBP1c signaling pathway.