Another study using apolipoprotein E (ApoE) knockout mice, which is an animal model of atherosclerosis, further indicated that the administration of OC improved vascular endothelium-dependent relaxation by the increase in endothelial nitric oxide synthase (eNOS) phosphorylation and the activation of the PI3K/Akt signaling pathway [114]. Here, APOE is linked to atherosclerosis.