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. 2017 Jan 13;13(2):404–422. doi: 10.1080/15548627.2016.1263776

Figure 4.

Figure 4.

Inhibition of mitochondria fission attenuates oxidative stress and endothelial dysfunction in prkaa2−/− mice. (A) WT and prkaa2−/− mice were injected with control (siCtrl) or siDnm1l (5 mg/kg). Four d after treatment, frozen sections of carotid artery were incubated with dihydroethidium (DHE; 5 µM) for 30 min. Representative fluorescence microscopic images of DHE-stained artery (A) and quantification of intensity grade showing with color lookup table (B). n = 5; *P < 0.05 vs. WT; #P < 0.05 vs. siCtrl. (C) Aortas were contracted with U46619 (30 nM). Endothelium-dependent vasodilator responses were measured in the presence of acetylcholine (Ach, 10−9 to 10−5 M). (D) Endothelium-independent vasodilator responses were measured in the presence of sodium nitroprusside (SNP, 10−10 to 10−6 M). n = 6 to 8; *P < 0.05 vs. WT; #P < 0.05 vs. siCtrl. (E and F) WT and prkaa2−/− mice were treated with mdivi-1 (1.2 mg/kg/d) or vehicle (DMSO) for 14 d. (E) Aortas were contracted with U46619. Endothelium-dependent vasodilator responses were measured in the presence of Ach (10−9 to 10−4 M). (F) Endothelium-independent vasodilator responses were measured in the presence of SNP (10−10 to 10−6 M). n = 6 to 8; *P < 0.05 vs. WT; #P < 0.05 vs. vehicle.