Chai Hui and Wo Like contributed equally to this work.
S-Allyl-L-Cysteine Sulfoxide Inhibits Tumor Necrosis Factor-Alpha Induced Monocyte Adhesion and Intercellular Cell Adhesion Molecule-1 Expression in Human Umbilical Vein Endothelial Cells
Article first published online: 20 JAN 2010
Copyright © 2010 Wiley-Liss, Inc.
The Anatomical Record
Volume 293, Issue 3, pages 421–430, March 2010
How to Cite
Hui, C., Like, W., Yan, F., Tian, X., Qiuyan, W. and Lifeng, H. (2010), S-Allyl-L-Cysteine Sulfoxide Inhibits Tumor Necrosis Factor-Alpha Induced Monocyte Adhesion and Intercellular Cell Adhesion Molecule-1 Expression in Human Umbilical Vein Endothelial Cells. Anat Rec, 293: 421–430. doi: 10.1002/ar.21070
- Issue published online: 17 FEB 2010
- Article first published online: 20 JAN 2010
- Manuscript Accepted: 14 JUL 2009
- Manuscript Received: 21 DEC 2008
Vol. 295, Issue 5, 715, Article first published online: 22 MAR 2012
- endothelial cells;
- S-Allyl-L-cysteine sulfoxide;
- tumor necrosis factor-alpha;
- intercellular cell adhesion molecule-1;
- superoxide anion;
- NADH oxidase
Garlic and its water-soluble allyl sulfur-containing compound, S-Allyl-L-cysteine Sulfoxide (ACSO), have shown antioxidant and anti-inflammatory activities, inhibiting the development of atherosclerosis. However, little is known about the mechanism(s) underlying the therapeutic effect of ACSO in inhibiting the formation of atherosclerostic lesion. This study aimed to investigate whether ACSO could modulate tumor necrosis factor-alpha (TNF-α)-induced expression of intercellular cell adhesion molecule-1, monocyte adhesion and TNF-α-mediated signaling in human umbilical vein endothelial cells. While TNF-α promoted the intercellular cell adhesion molecule-1 mRNA transcription in a dose- and time-dependent manner, ACSO treatment significantly reduced the levels of TNF-α-induced intercellular cell adhesion molecule-1 mRNA transcripts (P < 0.01). Furthermore, ACSO dramatically inhibited TNF-α triggered adhesion of THP-1 monocytes to endothelial cells and porcine coronary artery rings. Moreover, ACSO mitigated TNF-α induced depolarization of mitochondrial membrane potential and overproduction of superoxide anion, associated with the inhibition of NOX4, a subunit of nicotinamide adenine dinucleotide phosphate-oxidase, mRNA transcription. In addition, ACSO also inhibited TNF-α-induced phosphorylation of JNK, ERK1/2 and IκB, but not p38. Apparently, ACSO inhibited proinflammatory cytokine-induced adhesion of monocytes to endothelial cells by inhibiting the mitogen-activated protein kinase signaling and related intercellular cell adhesion molecule-1 expression, maintaining mitochondrial membrane potential, and suppressing the overproduction of superoxide anion in endothelial cells. Therefore, our findings may provide new insights into ACSO on controlling TNF-α-mediated inflammation and vascular disease. Anat Rec, 2010. © 2010 Wiley-Liss, Inc.