The effects of sesame lignans on adhesion molecules expression in tumor necrosis factor treated human aorta endothelial cells and the related mechanisms

• Main Authors: Ya-shi Kao, 高雅詩
• Other Authors: Wen-Huey Wu
• Format: Others
• Language: zh-TW
• Published: 2007
• Online Access: http://ndltd.ncl.edu.tw/handle/97486333188022269990

碩士 === 國立臺灣師範大學 === 人類發展與家庭學系 === 95 === The adhesion and migration of circulating leukocytes into the vessel wall is an early event in atherogenesis and the expression of cell adhesion molecules by the arterial endothelium plays a major role during atherogenesis. Antioxidants have been proposed to inhibit the expression of adhesion molecules and thereby attenuate the processes leading to atherosclerosis. In this study, the effects of antioxidant of sesame lignans, sesamol and sesamin, on the expression of adhesion molecules and the associated related mechanisms in tumor necrosis factor-α (TNF-α) treated human aortic endothelial cells (HAECs) were investigated. HAECs pretreated with sesamol (100μM) or sesamin (100 μM) for 24 h significantly suppressed cellular binding between the human monocytic leukemic cell line-U937 and TNF-α treated HAECs. Western blotting analysis showed that the treatment of sesamol (100μM) or sesamin (100 μM) for 24h significantly attenuated intercellular cell adhesion molecule-1 (ICAM-1) expression in HAECs under TNF-α stimulation. Phosphorylation studies on ERK1/2, JNK, and p38, three major subgroups of mitogen activator protein kinases, demonstrated that sesamin suppressed ERK1/2 and p38 phosphorylation. In addition, sesamol and sesamin significantly decreased the expression of NF-κB p65 and the activity of NF-κB by immunostaining and gel-mobility shift assay, respectively. These results provide the evidence that sesamin attenuated ICAM-1 expression caused by TNF-α stimulation and this inhibitory effect is mediated via downregulation of ERK1/2 and P38 phosphorylation and inactivation of NF-κB. These observation support the feasibility of sesame lignans administration is as a means of protection against endothelial dysfunction and inflammation.