L02脂肪变模型中氧化应激发生及羊栖菜多糖干预作用.docVIP

L02脂肪变模型中氧化应激发生及羊栖菜多糖干预作用 　　[摘要] 目的 建立人正常肝细胞株（L02）脂肪变模型，探讨软脂酸（PA）对肝细胞氧化应激的作用及羊栖菜多糖（SFPS）对脂肪变肝细胞氧化还原系统的影响。 方法 采用0.5 mmol/L的PA诱导L02细胞建立脂肪变模型，并予以不同浓度（25、50、100 μg/mL）SFPS进行干预。Annexin V-FITC标记法检测细胞的凋亡，MTT比色法检测细胞增殖活力，测定细胞内过氧化产物丙二醛含量（MDA）和超氧化物歧化酶（SOD）。 结果 SFPS可抑制PA对L02细胞增殖活性的下降和凋亡率的上升，降低MDA含量，升高SOD水平，不同浓度组间比较差异有统计学意义且具有剂量依赖性。 结论 L02细胞脂肪变性时发生明显的氧化应激，羊栖菜多糖能在一定程度上减轻氧化损伤、抗细胞凋亡。 　　[关键词] 羊栖菜多糖；氧化应激；脂肪肝；软脂酸 　　[中图分类号] R575 [文献标识码] A [文章编号] 1673-9701（2017）34-0017-03 　　The occurrence of oxidative stress in L02 fatty model and the intervention of sargassum fusiforme polysaccharide 　　WU Limin XIA Shenglong SHEN Sujian XIA Xuanping XUE Zhanxiong JIANG Yi 　　Department of Gastroenterology， the Second Affiliated Hospital of Wenzhou Medical University， Wenzhou 325000， China 　　[Abstract] Objective To establish a model of fatty degeneration in human normal liver cell line（L02） and to investigate the effect of palmitate（PA） on oxidative stress in hepatocytes and the effect of SFPS on the redox system of fatty liver cells. Methods L02 cells were induced by 0.5 mmol/L PA to establish a model of fatty degeneration， and were treated with different concentrations of SFPS（25， 50， 100 μg/mL）. Cell apoptosis was detected by Annexin V-FITC labeling method. Cell proliferation activity was measured by MTT colorimetric assay. Intracellular peroxide products including malondialdehyde（MDA） and superoxide dismutase（SOD） were measured. Results SFPS could inhibit the decrease of proliferation activity and apoptosis rate of L02 cells， decrease the content of MDA and increase the level of SOD， and the difference was statistically significant among different concentration groups and dose-dependent. Conclusions The oxidative stress occurs in the fatty degeneration of L02 cells. Sargassum fusiforme polysaccharide can alleviate oxidative damage and resist apoptosis to a certain extent. 　　[Key words] Sargassum fusiforme polysaccharide； Oxidative stress； Fatty liver； Palmitic acid非酒精性脂肪性肝病（non-alcoholic fat