The main findings of our study were: (i) oxLDL-induced endothelial dysfunction in primary HUVECs was efficiently prevented by Dp pretreatment through counteracting the mitochondrial apoptotic pathway; (ii) Dp was apparently taken-up by HUVECs and persistently preserved in blood vessels; and (iii) Dp uptake by VECs and its inhibitive effects on mitochondrial dysfunction were dependent on SGLT1 transport activity (Fig. 8). This evidence concerns the gene SLC5A1 and endothelial dysfunction.