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. 2022 Dec 6;11(23):e027538. doi: 10.1161/JAHA.122.027538

Figure 7. The increased endothelium‐dependent relaxation and the decreased superoxide level in Control‐HFHSD but not in EE2KO‐HFHSD mice with S18886.

Figure 7

Vascular relaxation of aortic rings of HFHSD‐fed control mice (A) and EE2KO (B) mice treated with BQ123, S18886, and U0126 (Control‐HFHSD, n=9; EE2KO‐HFHSD, n=7) and BQ123 (A and B) (Control‐HFHSD, n=9; EE2KO‐HFHSD, n=7), S18886 (A and B) (Control‐HFHSD, n=9; EE2KO‐HFHSD, n=7) and U0126 (A and B) (Control‐HFHSD, n=9; EE2KO‐HFHSD, n=10). Error bars represent SEM. *P<0.05, **P<0.01, ***P<0.001 (compared with controls). Dihydroethidium staining of aortic rings with BQ123, S18886, and U0126 (C) and quantification of dihydroethidium fluorescence intensity of Control‐HFHSD (D) (saline, n=8; BQ123, n=8; S18886, n=7; U0126, n=7) and EE2KO‐HFHSD (E) (n=6 per group) mice. Scale bar, 50 μm. Error bars represent SEM. Vascular relaxation was analyzed by 2‐way ANOVA with repeated measures followed by the post hoc Bonferroni correction for multiple comparisons (A and B). Between‐group differences were compared by 1‐way ANOVA (D and E). *P<0.05, **P<0.01, ***P<0.001. a.u. indicates arbitrary unit; EE2KO, endothelial‐specific extracellular signal‐regulated kinase 2 knockout; and HFHSD, high‐fat/high‐sucrose diet.