2008
DOI: 10.1271/bbb.70434
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Garlic (Allium sativum) Extract Inhibits Lipopolysaccharide-Induced Toll-Like Receptor 4 Dimerization

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Cited by 48 publications
(28 citation statements)
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“…Further investigation demonstrates that curcumin inhibits both ligand-induced and ligandindependent dimerization of TLR4 and reduces TLRs-mediated signaling pathways [50]. Similar results have been also obtained from isoliquiritigenin and some other garlic components, which all inhibit TLR4 dimerization and prevented subsequent signaling events [51,52]. These compounds may represent effective agents for balancing inflammatory disorder.…”
Section: Targeting On Tlrs Receptorssupporting
confidence: 58%
“…Further investigation demonstrates that curcumin inhibits both ligand-induced and ligandindependent dimerization of TLR4 and reduces TLRs-mediated signaling pathways [50]. Similar results have been also obtained from isoliquiritigenin and some other garlic components, which all inhibit TLR4 dimerization and prevented subsequent signaling events [51,52]. These compounds may represent effective agents for balancing inflammatory disorder.…”
Section: Targeting On Tlrs Receptorssupporting
confidence: 58%
“…38 Our previous study showed that garlic extract exerted anti-inflammatory activity by inhibiting Toll-like receptormediated signaling pathways at the receptor level. 23 In the present study, we isolated four sulfur compounds, 1-4 ( Fig. 1), exhibiting anti-inflammatory properties through activityguided procedures.…”
Section: Discussionmentioning
confidence: 92%
“…22 We previously showed that garlic extract exerts antiinflammatory activity by inhibiting the LPS-induced Tolllike receptor-4 dimerization followed by the suppression of NF-jB transcriptional activity and the expression of iNOS and cyclooxygenase (COX)-2. 23 NO synthase (NOS) catalyzes the oxidative deamination of l-arginine to produce NO. Three isoforms of NOS have been identified: endothelial NOS, neuronal NOS, and iNOS.…”
Section: Introduction Gmentioning
confidence: 99%
“…The production of NO and prostaglandin E2 were also inhibited. These authors speculated that sulfured compounds in EAG might interact with cysteine residues in TLR4 to form disulfide bonds for receptor dimerization, then leading to the inhibition of TLR4 (Youn et al, 2008). It has been also demonstrated that compounds with thiol binding affinity inhibit the LPS-induced dimerization (Youn et al, 2006).…”
Section: Toll-like Receptor-4 Dimerization As a Potential Sac's Targetmentioning
confidence: 99%