JOURNAL ARTICLE

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

Chai Hui, Wo Like, Fu Yan, Xie Tian, Wang Qiuyan, Huang Lifeng
Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology 2010, 293 (3): 421-30
20091890
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-alpha)-induced expression of intercellular cell adhesion molecule-1, monocyte adhesion and TNF-alpha-mediated signaling in human umbilical vein endothelial cells. While TNF-alpha promoted the intercellular cell adhesion molecule-1 mRNA transcription in a dose- and time-dependent manner, ACSO treatment significantly reduced the levels of TNF-alpha-induced intercellular cell adhesion molecule-1 mRNA transcripts (P < 0.01). Furthermore, ACSO dramatically inhibited TNF-alpha triggered adhesion of THP-1 monocytes to endothelial cells and porcine coronary artery rings. Moreover, ACSO mitigated TNF-alpha 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-alpha-induced phosphorylation of JNK, ERK1/2 and IkappaB, 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-alpha-mediated inflammation and vascular disease.

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