Fig 2: Immunostaining for peroxidases in moderately advanced diabetic nephropathy (a, b), FSGS (c), and IgAN (d). There is immunostaining for Prx1 (a), Prx2 (b), GPx1 (c), and catalase (d) in the podocytes of nonsclerotic glomeruli (arrows). Magnification: ×200. FSGS, focal segmental glomerulosclerosis; GPx, glutathione peroxidase; IgAN, IgA nephropathy; Prx, peroxiredoxin

Fig 3: Immunoblots showing expression of Prx1, Prx2, and GPx1 in podocytes in response to 250 µM PA. (a) Three hours following PA exposure, levels of Prx1, Prx2, and GPx1 proteins are significantly increased as compared with controls. (b) Quantitative analysis of Prx1, Prx2, and GPx1 from three experiments is shown. (c) Sixteen hours following PA exposure, the levels of these proteins are significantly decreased as compared with controls. (d) Quantitative analysis of Prx1, Prx2, and GPx1 from three experiments is shown. Results are mean ± SD (*P < 0.05 vs. control). BSA, bovine serum albumin; GPx, glutathione peroxidase; PA, palmitic acid; Prx, peroxiredoxin

Fig 4: Immunostaining for peroxidases and TGF‐β1. In controls, there is no staining for Prx1 (a), Prx2 (c), GPx1 (e), catalase (g), and TGF‐β1 (i). In the cases of advanced diabetic nephropathy, there is strong immunostaining for Prx1 (b), Prx2 (d), GPx1 (f), catalase (h), and TGF‐β1 (j) in the podocytes mainly overlying the lesions of nodular sclerosis (arrows). Magnification: ×200. GPx, glutathione peroxidase; Prx, peroxiredoxin; TGF‐β1, transforming growth factor‐β1