Fig 1: Anti-VEGF-A treatment modulates endothelial protein expression in APP/PS1 mice. ELISA measurements of VEGF-A (A) and eNOS (B) concentrations after 2 weeks of anti-VEGF-A treatment or saline control injections in APP/PS1 and wild-type (WT) mice (APP/PS1–saline: n = 6, APP/PS1–anti-VEGF-A: n = 6 (7), WT–saline: n = 9, WT–anti-VEGF-A: n = 5 (6); one-way ANOVA with Tukey’s post hoc multiple comparison correction to compare across groups: APP/PS1–saline (VEGF-A) versus APP/PS1–anti-VEGF-A (VEGF-A) P < 0.075, WT–saline (VEGF-A) versus WT–anti-VEGF-A (VEGF-A) P = 0.81, APP/PS1–saline (VEGF-A) versus WT–saline (VEGF-A) P < 0.05, APP/PS1–anti-VEGF-A (VEGF-A) versus WT–saline (VEGF-A) P = 0.93, APP/PS1–saline (eNOS) versus APP/PS1–anti-VEGF-A (eNOS) P < 0.01, WT–saline (eNOS) versus WT–anti-VEGF-A (eNOS) P < 0.01, APP/PS1–saline (eNOS) versus WT–saline (eNOS) P < 0.05). (C) Z-projection of confocal microscopy image stacks from representative cortical areas from mice of all four groups, revealing increased occludin density in anti-VEGF-A-treated APP/PS1 mice as compared to saline-injected APP/PS1 mice. Integrated density of occludin fluorescence as a function of the integrated density of the endothelial cell marker Glut-1 in the cortex (C) and hippocampus (D) (APP/PS1–saline: n = 3, APP/PS1–anti-VEGF-A: n = 3, WT–saline: n = 3, WT–anti-VEGF-A: n = 3; one-way ANOVA with Tukey’s post hoc multiple comparison correction to compare across groups: APP/PS1–saline cortex versus APP/PS1–anti-VEGF-A cortex P = 0.0006, saline WT cortex versus WT–anti-VEGF-A cortex P = 0.53, APP/PS1–saline cortex versus WT–saline cortex P = 0.0005, APP/PS1–anti-VEGF-A cortex versus WT–saline cortex P > 0.99, APP/PS1–saline hippocampus versus APP/PS1–anti-VEGF-A hippocampus P = 0.0004, WT–saline hippocampus versus WT–anti-VEGF-A hippocampus P > 0.99, APP/PS1–saline hippocampus versus WT–saline hippocampus P = 0.0002, APP/PS1–anti-VEGF-A hippocampus versus WT–saline hippocampus P > 0.99). Each point represents one mouse and the red horizontal represents the median. Sex differences are indicated by colour, with black data-points representing females and blue representing males.
Fig 2: KYP-2047 treatment on VEGF/a-SMA expression and eNOS levels. VEGF/a-SMA ratio expression was analyzed by Western blot, suggesting an increment of this marker in CVI group, compared to control animals (A), see the densitometric units score (B); treatment with KYP-2047 significantly reduced VEGF/a-SMA expression (A), see the densitometric units score (B). ELISA kit for eNOS expression on saphene vein samples was performed; treatment with KYP-2047 (10 mg/kg, i.p.) significantly reduced IL-8 quantification (C), compared to the high amount of eNOS released in the CVI-damaged groups (C). Data represent the means of at least three independent experiments. One-way ANOVA followed by Bonferroni post-hoc. *** p < 0.001 versus Sham; ### p < 0.001 versus CVI.
Supplier Page from Abcam for Mouse eNOS ELISA Kit