High glucose or 12(S)-HETE remarkably increased transendothelial dextran transport, and in combination it was increased further. Addition of the 12/15-LO inhibitor, CDC, partially suppressed dextran transport [1].

The high glucose and 12(S)-hydroxyeicosatetraenoic acid (HETE) could alter vascular endothelial (VE)-cadherin and β‐catenin phosphorylation levels, but did not alter total protein expression. However, the 12/15-LO inhibitor, Cinnamyl-3,4-dihydroxy-α-cyanocinnamate (CDC), antagonized the effect of high glucose on protein phosphorylation to mitigate destruction of the endothelial cell barrier, and the mouse diabetes mellitus model further confirmed these conclusions [1].