Fig. 7.

Smad3 knockdown attenuates acute kidney injury sensitivity in STZ-induced diabetic mice.

A. Schematic diagram illustrates the animal experimental design; B and C. mRNA and protein levels of Smad3; D. urinary albumin/creatinine ratio; E. Renal tissues stained with periodic acid-Schiff and quantification of tubular damage. Scale bars = 100 μm; F. BUN assay; G. Serum Creatinine assay; H. Western blot analysis showed protein expression of KIM-1; I. Immunohistochemistry and quantitative analysis of KIM-1; Scale bars = 100 μm; J. Quantitative real-time PCR detected the mRNA levels of KIM-1. 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 < 0.001 compared to ND group; ^ϕϕP < 0.01, ^ϕϕϕP < 0.001 compared to EV-I/R group; ^@@@P < 0.001 as indicated in Fig. 7. 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.