Research Paper Volume 16, Issue 4 pp 3302—3331

Figure 1. Inhibition of OS ameliorates the symptoms of DN in rats. (A–C) The body weights, renal index, and FBG levels of rats in each group. (D, E) Plasma TC, TG, Scr, BUN, UM, and ACR of rats in each group using enzymatic colorimetric assay and ELISA. (F–H) Histopathological examinations in the kidney tissues of rats in each group using HE, Masson, and PAS staining (scale bar = 20 μm). (I) The expression of α-SMA and TGF-β1 in the kidney tissues of rats in each group using immunohistochemistry (scale bar = 20 μm). (J) The expression of fibronectin and collagen IV in the kidney tissues of rats in each group using western blotting. (K) Cell apoptosis in the kidney tissues of rats in each group using TUNEL assay (scale bar = 20 μm). To explore the role of OS in DN development, 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; FBG: fasting blood-glucose; TC: total cholesterol, TG: triglyceride; BUN: blood urea nitrogen; Scr: serum creatinine; UM: urinary microalbumin; ACR: albumin to creatinine ratio; ELISA: enzyme-linked immunosorbent assay; HE: hematoxylin-eosin; PAS: periodic acid-Schiff; α-SMA: alpha-smooth muscle actin; TGF-β1: transforming growth factor beta 1; TUNEL: terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling; ROS: reactive oxygen species; NAC: N-Acetylcysteine.