In addition, both HT and metabolites (1, 2, 5, and 10 μM) provided protection against endothelial dysfunction in human aortic endothelial cells (HAECs) co-incubated with TNF-α by significantly reducing the secretion of E-selectin, P-selectin, ICAM-1, and VCAM-1, and HT metabolites further reduced levels of monocyte chemoattractant protein 1 (MCP-1) [83]. This evidence concerns the gene CCL2 and endothelial dysfunction.