摘要:
目的 研究硝苯吡啶对HK-2细胞铁超载引起的氧化应激的作用和可能的机制.方法 HK-2细胞分成空白组、铁超载组、硝苯吡啶组和共处理组,用柠檬酸铁铵和(或)硝苯吡啶处理细胞24 h后检测细胞丙二醛(MDA)含量、总超氧化物歧化酶(T-SOD)活性,谷胱甘肽(GSH)含量,细胞内铁含量以及二价金属离子转运蛋白1(DMT1)和膜铁转运蛋白1(FPN1)的表达.结果 与铁超载组相比硝苯吡啶组和共处理组MDA含量降低(P<0.05),T-SOD活性增加(P<0.05),GSH含量增加(P<0.05),细胞内铁含量降低(P<0.05),DMT1表达增加(P<0.05),FPN1表达增加(P<0.05).结论 硝苯吡啶在铁超载HK-2细胞的氧化应激中有保护作用,这一作用与硝苯吡啶促进DMT1和FPN1的表达、降低细胞内铁含量有关.%Objective To investigate the effect and the mechanism of nifedipine on oxidative stress trip-ping by iron-overload of HK-2 cells. Methods The cells were divided into 4 groups,blank group,iron overload group,nifedipine group and FAC with nifedipine co-treatment group. Cells were treated with FAC or/and nifedipine for 24 hours,and then malonaldehyde (MDA) content,superoxide dismutase (T-SOD) activity,glutathione (GSH) content,intracellular iron content and expression of DMT1 and FPN1 protein were evaluated. Results Compared to the iron overload group,both nifedipine treatment and co-treatment decreased the content of MDA (P < 0.05),increased the activity of SOD(P < 0.05),increased the content of GSH(P < 0.05),reduced the intracellular iron content(P<0.05),increased the expression of DMT1(P<0.05),and increased the expression of FPN1(P < 0.05). Conclusion Nifedipine plays a protective role against oxidative stress induced by iron-overload in HK-2 cells,and it is related to promote DMT1 and FPN1 protein expression and reduce intracellular iron content.