Abstract: Objective Investigates the potentials mechanisms that HTL promotes human umbilical vein endothelial cells (HUVECs) via endoplasmic reticulum stress pathway. Methods Detect the expression of NF-κB p65 in the rat thoracic aortic dissection tissue treated by HTL. Culture HUVECs, dealing with HTL on time dependent and does dependent. We detect the expression of endoplasmic reticulum stress protein Bip and Chop. Meanwhile we detect the expression of adhesive protein VCAM-1 and ICAM-1. Use the endoplasmic reticulum stress agonist and inhibitor deal with HUVEC, respectively. Then detect the affection of endoplasmic reticulum stress agonist and inhibitor on the expression of the adhesive protein in HUVECs induced by HTL, respectively. Use the protein interaction prediction tool STRING predicts the interaction between endoplasmic reticulum stress protein and adhesive protein. Results HTL induce the endothelial injury in isolated vessels; HTL increase the expressions of endoplasmic reticulum stress protein Bip and Chop in HUVECs (n=3,P<0.05); HTL upregulates the expressions of adhesive protein VCAM-1 and ICAM-1 in HUVECs (n=3,P<0.05); Endoplasmic reticulum stress agonist promotes the expression of adhesive protein VCAM-1 and ICAM-1 in HUVECs (n=3,P<0.05); Endoplasmic reticulum stress inhibitor dowmregulates the expression of adhesive protein VCAM-1 and ICAM-1 in HUVECs (n=3,P<0.05)；The protein interaction prediction tool STRING predicts the endoplasmic reticulum stress protein and adhesive protein have interactions. Conclusion: HTL might promote endothelial cell adhesion via endoplasmic reticulum stress pathway.

Key words: Key words: HTL, Endoplasmic reticulum stress, Adhesion molecule, endothelial cell adhesion