基础医学与临床 ›› 2015, Vol. 35 ›› Issue (1): 69-73.

• 研究论文 • 上一篇    下一篇

丙二醛通过抑制Nrf2/ARE促进肾小球系膜细胞凋亡

赵璐1,孙俊波2,金小琴2   

  1. 1. 河南中医学院第三附属医院
    2. 河南中医学院 第三附属医院
  • 收稿日期:2014-04-01 修回日期:2014-07-22 出版日期:2015-01-05 发布日期:2014-12-30
  • 通讯作者: 孙俊波

MDA accelerate the glomerular mesangial cell apoptosis via inhibition of Nrf2/ARE

  • Received:2014-04-01 Revised:2014-07-22 Online:2015-01-05 Published:2014-12-30

摘要: 目的 探索丙二醛(MDA)对糖尿病肾病的影响机制。方法 用终浓度为0、1 、5、10和50 μmol/L的MDA处理肾小球系膜细胞(GMC),MTT法检测细胞活性,AnnexinV-FITC法检测细胞凋亡, RT-PCR和Western blot法检测Nrf2,HO-1和γGCL表达。结果 MDA 剂量依赖的抑制肾小球系膜细胞的活性。MDA浓度为5 μmol/L可诱导细胞内大量活性氧(ROS)产生(P<0.05),抗氧化剂tBHQ可缓解MDA诱导的细胞活性的下降。MDA抑制了抗氧化反应原件(ARE)HO-1和γGCL的表达,以及Nrf2的表达水平(P<0.05)。结论 MDA可通过抑制Nrf2/ARE来调控ROS生成,抑制肾小球系膜细胞的活性。

关键词: 丙二醛, 糖尿病肾病, 肾小球系膜细胞, ROS, Nrf2

Abstract: Objective To explore the function of MDA on diabetic nephropathy. Methods Glomerular mesangial cells (GMC) were pretreated with MDA at a final concentrations of 0 μmol/L, 1 μmol/L, 5 μmol/L, 10 μmol/L and 50 μmol/L. MTT assay was used to observe the viability of GMC) . AnnexinV-FITC was used to evaluate effect of MDA on cell apoptosis. RT-PCR and western blot were used to analyze the expression of Nrf2, HO-1 and γGCL. Results MDA treatment inhibited GMC viability in a dose-dependent manner. MDA at the concentration of more than 5 μM induced mass production of ROS in GMC (P<0.05). In addition, antioxygen of tBHQ could relieve MDA-induced decreased of cell viability. MDA inhibited the expression of HO-1, γGCLand Nrf2 (P<0.05). Conclusions This study confirmed that MDA inhibited the GMC viability and promotes the cell apoptosis by ROS production through inhibiting Nrf2/HO-1-γGCL.

Key words: malondialdehyde, Diabetic Nephropathy, glomerular mesangial cell, ROS, Nrf2