Fig. 8.

Smad3 knockdown protects against renal inflammation, oxidative stress and apoptosis in STZ-induced diabetic mice.

A. Immunohistochemistry and quantitative analysis of TNF-α and F4/80 + macrophages; Scale bars = 100 μm and 50 μm; B. Real-time PCR detected mRNA levels of TNF-α and IL-1β; C. Western blot analysis showing protein expression of NOX4; D-F. Level of GSH, SOD and MDA; G. Western blot analysis showing protein expression of p-Smad3, Smad3, p-Smad2, Smad2, P-p53, p53 and cleaved caspase-3. H. Representative micrographs show terminal deoxynucleotidyl transferase–mediated dUTP nick end-labeling (TUNEL)-positive cells and proliferating cell nuclear antigen (PCNA) (green nuclei)-positive cells in different groups; Scale bars = 100 μm; I. The proliferation/apoptosis ratio. Data represent the mean ± S.E.M. for 6–8 mice. *P < 0.05, **P < 0.01, ***P < 0.001 compared to S group; ^#P < 0.05, ^##P < 0.01, ^###P < 0.001 compared to ND group; ^ϕP < 0.05, ^ϕϕP < 0.01, ^ϕϕϕP < 0.001 compared to EV-I/R group. ND: non-diabetic mice; DM: STZ-induced diabetic mice; I/R and DM + I/R: non-diabetic mice and STZ-induced diabetic mice were subject to ischemia reperfusion injury; EV: empty vector; KD: knockdown; S: Sham. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)