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. 2012 Apr 5;112(12):2110–2120. doi: 10.1152/japplphysiol.01383.2011

Fig. 3.

Fig. 3.

Cardiac apoptosis in SHR is prevented by Ena. A: representative blots and average data of the proapoptotic and antiapoptotic proteins Bax and Bcl-2, respectively, and the 17-kDa cleavage product of caspase-3 from control rats, SHR, and SHR treated with Ena. GAPDH signals were used as loading controls. The increased ratio Bax/Bcl-2, used as an apoptotic index, and caspase-3 activation in SHR, are prevented by Ena treatment. B: typical photographs of terminal deoxynucleotidyl transferase dUTP-mediated nick-end labeling (TUNEL) assay and 4′,6-diamidino-2-phenylindole dihydrochloride (DAPI) staining of control, SHR, and SHR treated with Ena. The mean values of TUNEL-positive cells normalized by total DAPI-stained nuclei in the bar graph below indicate that the increment in apoptosis in SHR is prevented by blocking RAAS axis. Values are means ± SE; n, no. of animals in each experimental group (in parentheses). *P < 0.05 vs. control. §P < 0.05, +Ena vs. SHR.