丙二醛通过抑制Nrf2／ARE促进肾小球系膜细胞凋亡

摘要

Objective To explore the function of MDA on diabetic nephropathy .Methods Glomerular mesangial cells ( GMC) were pretreated with MDA at a final concentrations of 0μmol/L, 1μmol/L, 5μmol/L, 10μmol/L and 50 μmol/L.MTT assay was used to examine 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 Nrf 2, HO-1 andγGCL.Results MDA treatment inhibited GMC viability in a dose-dependent manner .MDA at the concentration of more than 5 μmol/L induced mass production of ROS in GMC ( P<0.05 ) .In addition , antioxygen of tBHQ may relieve MDA-induced reduction of cell viability .MDA inhibited the expression of HO-1 , γGCLand Nrf2 ( P <0.05 ) .Conclusions MDA inhibites GMC viability and promotes the cell apoptosis by ROS production through in-hibiting Nrf2/HO-1-γGCL.%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50μmol／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5μmol／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。