硝苯吡啶在铁超载HK-2细胞氧化应激中的作用及机制  

Effects of nifedipine on oxidative stress causing by iron-overload in HK-2 cells

作　　者：吕小梅 冉兵 杨茂 李雪森 蔺艳 LU Xiaomei, RAN Bing, YANG Mao, LI Xuesen, LIN Yan.(Department of physiology and research, Southwest Medical University, Luzhou, 646000, Chin)

机构地区：[1]西南医科大学生理学教研室,四川泸州646000 [2]西南医科大学肿瘤医学研究所,四川泸州646000

出　　处：《实用医学杂志》2018年第12期1938-1941,共4页The Journal of Practical Medicine

基　　金：四川省卫生厅项目(编号:110330)

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 overloadgroup,nifedipine group and FAC with nifedipine co-treatment group. Cells were treated with FAC or/and nifedipinefor 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 theintracellular iron content（P〈0.05）,increased the expression of DMT1（P〈0.05）,and increased the expressionof 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 intracellulariron content.

关 键 词：铁超载 硝苯吡啶 HK-2细胞 氧化应激 

分 类 号：R96[医药卫生—药理学]