黑灵芝多糖对丙烯酰胺诱导小肠上皮细胞氧化损伤的保护作用

摘要

目的:研究黑灵芝多糖对丙烯酰胺(acrylamide,AA)所致的小肠上皮细胞氧化损伤的保护作用.方法:构建AA诱导小肠上皮细胞(intestinal epithelial cells,IEC).-6氧化损伤型,采用噻唑蓝比色法检测黑灵芝多糖对IEC-6氧化损伤的保护作用;同时测定细胞培养液中乳酸脱氢酶(lactate dehydrogenase,LDH)的漏出量,以及测定细胞中超氧化物歧化酶(superoxide dismutase,SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)及丙二醛(malondialdelyde,MDA)水平.结果:与正常对照组相比,不同质量浓度的黑灵芝多糖对细胞增殖影响无显著性差异.与模型(AA)组相比,不同质量浓度的黑灵芝多糖溶液能够明显减轻AA对细胞的毒害作用,提高细胞生存率,降低细胞培养液中LDH的释放;降低MDA含量,提高细胞SOD和GSH-Px活性.结论:黑灵芝多糖可以通过提高细胞内抗氧化酶系的活性和抗氧化物质GSH-Px活性从而有效地减弱AA诱导的小肠上皮细胞氧化损伤.%Objective:To investigate the protective effect of Ganoderma atrum polysaccharides (GAP) against oxidative injury induced by acrylamide (AA) in intestinal epithelial cells (IEC)-6.Methods:The MTT assay was used to evaluate the proliferation of IEC-6.After cultivation,the cells and culture medium were collected for determining the activities of lactate dehydrogenase (LDH),malondialdelyde (MDA),superoxide dismutase (SOD) and reduced glutathione peroxidase (GSH-Px).Results:GAP had no toxic effect on the cultured IEC-6 at the tested concentrations.Compared with the AA-treated group,GAP significantly attenuated AA-induced oxidative damage and increased cell viability by decreasing LDH activity and MDA content,and increasing SOD and GSH-Px activities in IEC-6 line.Conclusion:These results suggested that GAP showed a protective effect against AA-induced oxidative damage in IEC-6 through inhibiting lipid peroxidation,and increasing antioxidant system activity.