FXa-induced endothelial dysfunction in aortic rings (P < 0.001) and eNOS<sup>Ser1177</sup> phosphorylation (P < 0.05) in HCAEC were partially ameliorated by a JNK inhibitor.
DJC therapy exhibited a potent antioxidant activity and effectively prevented the endothelial dysfunction (ED) manifested by promoting p-eNOS expression and enhancing NO release, decreasing lipid deposition (Oil-red O staining, CPT1b and ACC) and inflammation (IL-1β, TNFα, CD68 and p-JNK), alleviating oxidative and ER stress, and decreasing the apoptosis of endothelial cells (TUNEL, BCL-2 and BAX) induced by HFD and palmitic acid respectively.