Skip to main content
. 2013 Nov 14;170(7):1396–1409. doi: 10.1111/bph.12346

Figure 3.

Figure 3

PDE5 inhibition suppressed ER stress and ER stress-mediated apoptosis in hypertrophic and failing hearts. (A) PDE5 inhibition by sildenafil (Sil) significantly attenuated the isoprenaline (Iso)-induced increase in ANP, PDE5, P-PERK, GRP78 and XBP1s in rats. Proteins were normalized to GAPDH. *P < 0.05 versus saline. #P < 0.05 versus isoprenaline. (B) Sildenafil markedly attenuated the TAC-induced ER stress in mice. *P < 0.05 versus sham. #P < 0.05 versus TAC. (C) Immunohistochemical analyses of KDEL in rat hearts. Scale bar: 100 μm. (D) CHOP was increased in isoprenaline rats, and sildenafil treatment reduced expression of CHOP. CHOP was normalized to GAPDH. *P < 0.05 versus saline. #P < 0.05 versus Iso. (E) Sildenafil treatment reduced the TAC-induced increase of CHOP. *P < 0.05 versus sham. #P < 0.05 versus TAC. (F) Representative images of TUNEL staining showing cardiomyocyte apoptosis and quantitative analysis of TUNEL-positive myocardial cells in rats. Scale bar: 50 μm. Data are expressed as mean ± SEM (n = 5). *P < 0.05 versus saline. #P < 0.05 versus isoprenaline.