Research Paper Volume 16, Issue 4 pp 3302—3331

Figure 2. Inhibition of OS rescues mitochondrial dysfunction in DN rats. (A, B) Assessment of the levels of MDA, SOD, GPX, and CAT in the kidney tissues and plasma of rats in each group using ELISA. (C, D) ROS production and ATP release in the kidney tissues of rats in each group. (E) Observation of mitochondrial morphology under TEM (scale bar = 500 nm). (F) Mitochondrial ROS production in the kidney tissues of rats in each group (scale bar = 20 μm). (G) The expression of Drp1, Fis1, OPA1, and Mfn1 in the kidney tissues of rats in each group using western blotting. To figure out the impact of OS on mitochondrial function in DN, DN rats were treated with or without the ROS inhibitor, N-Acetylcysteine (NAC; 20 mg/kg) for eight successive weeks. Data were expressed as mean ± standard deviation (n = 6/group). ^**p < 0.01 vs. Control group; ^#p< 0.05 and ^##p < 0.01 vs. DN group. Abbreviations: OS: oxidative stress; DN: diabetic nephropathy; MDA: malondialdehyde; SOD: superoxide dismutase; GPX: glutathione peroxidase; CAT: catalase; ELISA: enzyme-linked immunosorbent assay; ROS: reactive oxygen species; ATP: adenosine triphosphate; TEM: transmission electron microscopy; NAC: N-Acetylcysteine.