Figure 10.

Deficiency of the redox-protein p66^Shc reduces inflammasome activation in diabetic nephropathy. In diabetic mice lacking the redox-protein p66^Shc levels of Nlrp3 (a–c) and cleaved IL-1β (c) are reduced in comparison with diabetic wild-type (WT) mice (streptozotocin model, 24 weeks of hyperglycemia). Immunohistochemical detection of Nlrp3 in glomeruli of diabetic WT and p66^Shc−/− mice (a), Nlrp3-positive cells detected by HRP-DAB reaction, brown; hematoxylin counterstain, blue; scale bar=20 μm; bar graph summarizing results of integrated optical density (IOD) of positive DAB stain (b); mean value±s.e.m. Number of mice (a–c) in each group is shown in parentheses in b, and representative immunoblots in c; **P<0.01. AU, arbitrary units; DM, diabetic mice; IL, interleukin; Nlrp3, nucleotide-binding domain and leucine-rich repeat pyrin 3 domain.