Research Paper Volume 13, Issue 9 pp 12996—13005

Azilsartan ameliorates ox-LDL-induced endothelial dysfunction via promoting the expression of KLF2

Silencing of KLF2 abolished the effects of Azilsartan in occludin expression and endothelial permeability. Cells were transfected with KLF2 siRNA, followed by stimulation with ox-LDL (100 μg/mL) in the presence or absence of Azilsartan (6 μM) for 24 hours. (A) Successful knockdown of KLF2 as measured by western blot analysis. (B) Gene expression of occludin; (C) Endothelial monolayer permeability (****, P

Figure 8. Silencing of KLF2 abolished the effects of Azilsartan in occludin expression and endothelial permeability. Cells were transfected with KLF2 siRNA, followed by stimulation with ox-LDL (100 μg/mL) in the presence or absence of Azilsartan (6 μM) for 24 hours. (A) Successful knockdown of KLF2 as measured by western blot analysis. (B) Gene expression of occludin; (C) Endothelial monolayer permeability (****, P<0.0001 vs. vehicle group; ####, P<0.0001 vs. ox-LDL group; $$$$, P<0.0001 vs. ox-LDL+ Azilsartan group, N=5-6 for each group).