Figure 2.

The antifibrotic actions of RLX in the injured kidney were blocked by the AT₁R antagonist candesartan in vivo. (A) Representative Western blots of renal phosphorylated (phospho)-p44 and p42 MAPK (phospho-ERK1/2), total p44 and p42 MAPK (ERK1/2), nNOS, phospho-nNOS, TGF-β1, phospho-Smad2, total Smad2, α-SMA, L-MMP-13, and α-tubulin. (B) Representative images of immunohistochemically stained collagen I and collagen IV as well as total kidney collagen concentration in UUO-injured male C57B6J wild-type mice that were untreated for 5 days or treated with RLX (0.5 mg/kg per day) alone, or RLX (0.5 mg/kg per day) and candesartan cilexetil (2 mg/kg per day) from 2 days before injury until 5 days postinjury. Scale bar, 100 μm. Total p44 and p42 MAPK (ERK1/2), unphosphorylated Smad2, and α-tubulin blots (A) were included to demonstrate the quality and equivalent loading of protein samples. Also shown (B) are the mean±SEM total kidney collagen concentration (expressed as a percentage of the dry weight tissue) or renal collagen I and collagen IV staining (expressed as a percentage of the fractional area stained, respectively) (from n=5–6 animals per treatment group). *P<0.01 versus UUO-injured/untreated group; ^#P<0.01 versus UUO-injured/RLX-treated group.