Sesamin attenuates intercellular cell adhesion molecule-1 expression in vitro in TNF-α-treated human aortic endothelial cells and in vivo in apolipoprotein-E-deficient mice

被引:32
作者
Wu, Wen-Huey [2 ]
Wang, Shu-Huei [1 ]
Kuan, I-I [1 ]
Kao, Ya-Shi [2 ]
Wu, Pei-Jhen [1 ]
Liang, Chan-Jung [1 ]
Chien, Hsiung-Fei [3 ]
Kao, Chiu-Hua [2 ]
Huang, Ching-Jang [4 ]
Chen, Yuh-Lien [1 ]
机构
[1] Natl Taiwan Univ, Coll Med, Dept Anat & Cell Biol, Taipei 100, Taiwan
[2] Natl Taiwan Normal Univ, Dept Human Dev & Family Studies, Taipei, Taiwan
[3] Natl Taiwan Univ, Natl Taiwan Univ Hosp, Dept Surg, Taipei 100, Taiwan
[4] Natl Taiwan Univ, Coll Life Sci, Dept Biochem Sci & Technol, Taipei 100, Taiwan
关键词
Atherosclerosis; Endothelial cell; Intercellular cell adhesion molecule-1; NF-kappa B; Sesamin; TUMOR-NECROSIS-FACTOR; NF-KAPPA-B; RATS; ATHEROSCLEROSIS; OIL; INHIBITION; ALCOHOL; LIPIDS; HUR;
D O I
10.1002/mnfr.200900271
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Sesame lignans have antioxidative and anti-inflammatory properties. We focused on the effects of the lignans sesamin and sesamol on the expression of endothelial-leukocyte adhesion molecules in tumor necrosis factor-alpha (TNF-alpha)-treated human aortic endothelial cells (HAECs). When HAECs were pretreated with sesamin (10 or 100 mu M), the TNF-alpha-induced expression of intercellular cell adhesion molecule-1 (ICAM-1) was significantly reduced (35 or 70% decrease, respectively) by Western blotting. Sesamol was less effective at inhibiting ICAM-1 expression (30% decrease at 100 mu M). Sesamin and sesamol reduced the marked TNF-alpha-induced increase in human antigen R (HuR) translocation and the interaction between HuR and the 3'UTR of ICAM-1 mRNA. Both significantly reduced the binding of monocytes to TNF-alpha-stimulated HAECs. Sesamin significantly attenuated TNF-alpha-induced ICAM-1 expression and cell adhesion by downregulation of extracellular signal-regulated kinase 1/2 and p38. Furthermore, in vivo, sesamin attenuated intimal thickening and ICAM-1 expression seen in aortas of apolipoprotein-E-deficient mice. Taken together, these data suggest that sesamin inhibits TNF-alpha-induced extracellular signal-regulated kinase/p38 phosphorylation, nuclear translocation of NF-kappa B p65, cytoplasmic translocalization of HuR and thereby suppresses ICAM-1 expression, resulting in reduced adhesion of leukocytes. These results also suggest that sesamin may prevent the development of atherosclerosis and inflammatory responses.
引用
收藏
页码:1340 / 1350
页数:11
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