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. Author manuscript; available in PMC: 2015 Nov 1.
Published in final edited form as: Circ Heart Fail. 2014 Oct 2;7(6):1032–1041. doi: 10.1161/CIRCHEARTFAILURE.114.001260

Figure 5. LXRα/β dual agonists attenuated oxidative/nitrative stresses in ischemic/reperfused myocardium.

Figure 5

A–C. LXR activation attenuated oxidative stresses in ischemic/reperfused myocardium. A. Myocardial oxidative stress was measured utilizing confocal microscope with in-situ dihydroethidium stain (n=5–6, bar=25 μm). B. NADPH oxidase activity was determined by lucigenin-enhanced chemiluminescence (n=6–8; *P=0.005, †P=0.02 vs. vehicle). C. NADPH oxidase gp91phox gene expression was determined by real-time PCR (n=5–6; *P=0.02, †P=0.002 vs. vehicle). Results were normalized against GAPDH and converted to fold induction relative to sham-operated controls.

D–F. LXR activation attenuated nitrative stress in ischemic/reperfused myocardium. D. Myocardial nitrative stress was assessed via nitrotyrosine levels determined by immunohistochemistry (n=5–6, bar=25 μm). E. Myocardial nitrotyrosine content was determined by ELISA analysis (n=6–8; *P=0.02, †P=0.004 vs. vehicle). F. The gene expression of iNOS was determined by real-time PCR (n=5–6; *P=0.04, †P=0.005 vs. vehicle). Results were normalized against GAPDH and converted to fold induction relative to sham-operated controls. Abbreviations: 22(R)-HC, 22(R)-hydroxycholesterol; RLU, relative light units; iNOS, inducible nitric oxide synthase.