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