{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,30]],"date-time":"2025-12-30T22:59:01Z","timestamp":1767135541891,"version":"build-2238731810"},"reference-count":34,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2010,1,20]],"date-time":"2010-01-20T00:00:00Z","timestamp":1263945600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Anatomical Record"],"published-print":{"date-parts":[[2010,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Garlic and its water\u2010soluble allyl sulfur\u2010containing compound,\n                    <jats:italic>S<\/jats:italic>\n                    \u2010Allyl\u2010\n                    <jats:sc>L<\/jats:sc>\n                    \u2010cysteine Sulfoxide (ACSO), have shown antioxidant and anti\u2010inflammatory 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\u2010alpha (TNF\u2010\u03b1)\u2010induced expression of intercellular cell adhesion molecule\u20101, monocyte adhesion and TNF\u2010\u03b1\u2010mediated signaling in human umbilical vein endothelial cells. While TNF\u2010\u03b1 promoted the intercellular cell adhesion molecule\u20101 mRNA transcription in a dose\u2010 and time\u2010dependent manner, ACSO treatment significantly reduced the levels of TNF\u2010\u03b1\u2010induced intercellular cell adhesion molecule\u20101 mRNA transcripts (\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.01). Furthermore, ACSO dramatically inhibited TNF\u2010\u03b1 triggered adhesion of THP\u20101 monocytes to endothelial cells and porcine coronary artery rings. Moreover, ACSO mitigated TNF\u2010\u03b1 induced depolarization of mitochondrial membrane potential and overproduction of superoxide anion, associated with the inhibition of NOX4, a subunit of nicotinamide adenine dinucleotide phosphate\u2010oxidase, mRNA transcription. In addition, ACSO also inhibited TNF\u2010\u03b1\u2010induced phosphorylation of JNK, ERK1\/2 and I\u03baB, but not p38. Apparently, ACSO inhibited proinflammatory cytokine\u2010induced adhesion of monocytes to endothelial cells by inhibiting the mitogen\u2010activated protein kinase signaling and related intercellular cell adhesion molecule\u20101 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\u2010\u03b1\u2010mediated inflammation and vascular disease. Anat Rec, 2010. \u00a9 2010 Wiley\u2010Liss, Inc.\n                  <\/jats:p>","DOI":"10.1002\/ar.21070","type":"journal-article","created":{"date-parts":[[2010,1,20]],"date-time":"2010-01-20T14:53:40Z","timestamp":1263999220000},"page":"421-430","source":"Crossref","is-referenced-by-count":18,"title":["<i>S<\/i>\n                    \u2010Allyl\u2010\n                    <scp>L<\/scp>\n                    \u2010Cysteine Sulfoxide Inhibits Tumor Necrosis Factor\u2010Alpha Induced Monocyte Adhesion and Intercellular Cell Adhesion Molecule\u20101 Expression in Human Umbilical Vein Endothelial 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