Research Paper Volume 13, Issue 9 pp 12996—13005

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

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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).