Figure 3

TRPV1 activation ameliorates high-glucose-induced endothelial dysfunction in a UCP2-dependent manner. A: Representative immunofluorescence images showing the co-expression of TRPV1, PKA and UCP2 in the aortas from wild type mice, particularly in the endothelium (Bar denotes 50 μm). B and C: Acetylcholine (1 nmol/L to 10 μmol/L)-induced endothelium-dependent relaxation of isolated aortic artery rings from wild type and TRPV1^-/- mice, pre-incubated with normal-glucose for 12 hours (NG, glucose 5.5 mmol/L), high-glucose (HG, glucose 30 mmol/L), HG+capsaicin (HG+Cap, Cap 1 μmol/L), HG+Cap+KT5720 (2 μmol/L); **P<0.01 versus NG group; ##P<0.01 versus HG group; ΔΔP<0.01 versus HG+Cap group. Data are mean ± SEM. Each n=6. D and E: Nitroglycerin (1 nmol/L to 10 μmol/L) -induced endothelium-independent relaxation of isolated aortic artery rings from wild type and TRPV1^-/- mice, after cultured for 12 hours with NG, HG, HG+Cap. Data are mean ± SEM. Each n =6. F and G: Representative data that Acetylcholine- and nitroglycerin-induced relaxation in the presence or absence of capsaicin (Cap, 1 μmol/L) in isolated aortic arteries rings from UCP2^-/- mice and wild type (WT) mice under high-glucose condition(HG). **P<0.01 HG + Cap versus HG group of WT, #P<0.05 HG group of WT versus HG group of UCP2^-/-. Data are mean ± SEM. Each n=6.