Fig. 2

Effects of NCEH1 on vascular relaxation in HG-incubated or HFD-induced mouse aortae. (A) EDR in aortic rings from NG (mannitol, 25 mM) or HG (D-glucose (25 mM)-induced mouse aortae with or without NCEH1. (B) EDR in aortic rings from NG- or HG-induced mouse aortae after overexpression of NCEH1. (C) Endothelium-independent relaxation in aortic rings from NG- or HG-induced mouse aortae with or without NCEH1. (D) Endothelium-independent relaxation in aortic rings from NG- or HG-induced mouse aortae after overexpression of NCEH1. (E) EDR in aortic rings from normal diet- or HFD-induced mouse aortae with or without NCEH1. (F) EDR in aortic rings from normal diet- or HFD-induced mouse aortae after overexpression of NCEH1. (G) Endothelium-independent relaxation in aortic rings from normal diet- or HFD-induced mouse aortae with or without NCEH1. (H) Endothelium-independent relaxation in aortic rings from normal diet- or HFD-induced mouse aortae after overexpression of NCEH1. n = 6. *P < 0.05 versus Control (Con) or normal glucose (NG). †P < 0.05 versus HG or HFD. Differences between groups were assessed with ANOVA followed by Bonferroni post-hoc test (A-H). Relaxation at each concentration was expressed as the percentage of force in response to Phe. NCEH1, neutral cholesterol ester hydrolase 1; NG, normal glucose; HG, high glucose; Con, Control; HFD, high fat diet; Phe, phenylephrine; Ach, acetylcholine; SNP, sodium nitroprusside