Abstract
Novel peptides derived from chicken collagen hydrolysate (CCH) were confirmed to have a vasoprotective effect after ingestion and absorption to vessels; however, their endovascular mechanism of action required clarification. Therefore, using human umbilical vein endothelial cells (HUVECs), in which inflammation had been induced by tumor necrosis factor-α (TNF-α), we investigated the mechanism by which CCH-derived peptides inhibited the vascular inflammatory response. Expression of soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), and interleukin-8 (IL-8) in HUVECs was increased significantly by the addition of TNF-α, whereas treatment with proline-hydroxyproline (Pro-Hyp) and hydroxyproline-glycine (Hyp-Gly), which are present in human peripheral blood after ingestion of CCH, inhibited these increases. These peptides also reduced the mRNA expression of inducible nitric oxide synthase (iNOS) up-regulated by TNF-α. These results suggest that the vasoprotective effect of CCH-derived peptides is due to inhibition of endothelial inflammation.
