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. Author manuscript; available in PMC: 2012 Sep 15.
Published in final edited form as: J Pharmacol Sci. 2012 Jul 21;119(4):359–367. doi: 10.1254/jphs.12075fp

Fig. 3.

Fig. 3

Reno-protective effects of cilnidipine. Urinary protein excretion (A) and urinary albumin excretion (B). The vehicle group demonstrated substantial proteinuria and albuminuria compared with WKY. Cilnidipine significantly suppressed proteinuria and albuminuria in both the denervated and innervated groups. C) Representative images with desmin immunostaining (a – e, × 200) and PAS staining (f – j, × 200), as well as the quantitative comparisons between the groups. Podocyte injury revealed by desmin immunostaining was greater in the vehicle group (a) compared to WKY (e). Podocyte injury was significantly reduced with cilnidipine treatment in innervated (c) and denervated (d) rats. Denervation did not attenuate desmin staining in the glomeruli of the vehicle group (b). Glomerulosclerosis and extracellular matrix accumulation were revealed with PAS staining in the vehicle group (f) compared with WKY (j). Denervation attenuated the PAS staining (g). Cilnidipine treatment either in innervated (h) or denervated (i) animals prevented the increase in PAS staining. Denervation in cilnidipine-treated animals did not show additional attenuation. Scale bars: 100 μm. D) Transforming growth factor β1 (TGF-β1) mRNA expression. Expression of TGF-β1 mRNA was significantly higher in the vehicle group than in WKY. The increase in expression was significantly improved in both the cilnidipine-DNX and cilnidipine groups. All rats were uninephrectomized and fed the 4% NaCl–containing diet. *P < 0.05 vs. WKY, #P < 0.05 vs. the vehicle group. WKY: Wistar Kyoto rat, DNX: denervation.