泽漆醇提取物抗氧化活性及对油酸诱导HepG2细胞脂肪堆积的影响

Antioxidant Activity of Euphorbia helioscopia Ethanol Extract and Its Effect on Oleic Acid Induced Fat Accumulation in HepG2 Cells

为了探究泽漆醇提取物体外抗氧化作用及其对油酸诱导HepG2细胞脂肪堆积的影响。本研究采用浸渍法分别以25%、50%、75%甲醇和乙醇对泽漆粉末进行提取,评估不同泽漆提取物的体外抗氧化活性,并测定其总酚和总黄酮含量。建立HepG2细胞脂肪堆积模型,不同浓度(20、40、60μg/mL)泽漆50%乙醇提取物处理24 h,观察细胞内脂滴形成情况;测定细胞中甘油三脂(triglyceride,TG)含量、总谷胱甘肽(glutathione,GSH)、超氧化物歧化酶(superoxide dismutase,SOD)的活性及总抗氧化能力(total antioxidant capacity,T-AOC)。结果表明,泽漆醇提取物均具有抗氧化活性,且有浓度依赖性,其中50%乙醇提取物在一定浓度范围内抗氧化效果最佳(P<0.05),且总酚(8.813%±1.344%)和总黄酮(17.938%±0.819%)含量也较高。与模型组比较,泽漆50%乙醇提取物能够降低HepG2细胞内脂滴和TG值,提高细胞GSH、T-AOC含量和SOD活性(P<0.05),具有浓度依赖性。综上可知,50%乙醇提取物可以抑制油酸诱导的HepG2细胞脂肪堆积,并增强细胞内源性抗氧化能力。

In order to investigate the antioxidant effect of the extract of Euphorbia helioscopia in vitro and its effect on lipid accumulation in HepG2 cells induced by oleic acid.In this study,25%,50%,75%methanol and ethanol were used to extract the powder by immersion method.The antioxidant activi ties of the different extracts were assessed,and the levels of total phenols and total flavonoids were measured.To establish a model of lipid accumulation in HepG2 cells,the cells we re treated with 50%ethanol extract(at concentrations of 20,40,and 60µg/mL)for 24 h to observe the formation of lipid droplets.The triglyceride(TG)content,total glutathione(GSH),superoxide dismutase(SOD)activity,and total antioxidant capacity(T-AOC)in the cells were determined.The findings demonstrated that all extracts exhibited concentrationdependent antioxidant activity.Among them,the 50%ethanol extract exhibited the most potent antioxidant effect in a certain concentration range(P<0.05),with higher levels of total phenols(8.813%±1.344%)and total flavonoids(17.938%±0.819%).Compared with the model group,the 50%ethanol e xtract displayed a concentration-dependent ability to decrease lipid droplets and TG values in HepG2 cells,whi le increasing the levels of GSH,T-AOC,and SOD activity.Therefore,the 50%ethanol extract showed potential in inhibit ing oleic acid-induced fat accumulation in HepG2 cells and enhancing the endogenous antioxidant capacity of the cells.