Suppression of homodimerization of toll-like receptor 4 by isoliquiritigenin

Park, Se-Jeong; Youn, Hyung‐Sun

doi:10.1016/j.phytochem.2010.07.008

Cited by 39 publications

(35 citation statements)

References 30 publications

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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: 59%

TLRs as pharmacological targets for plant-derived compounds in infectious and inflammatory diseases

Liu¹,

Zheng²,

Zhou³

2011

International Immunopharmacology

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Section: Targeting On Tlrs Receptorssupporting

confidence: 59%

TLRs as pharmacological targets for plant-derived compounds in infectious and inflammatory diseases

Liu¹,

Zheng²,

Zhou³

2011

International Immunopharmacology

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“…Then, the observed suppression of the increase in TLR4 expression in the kidneys of rats fed with (−)-epicatechin could be due to: i) a prevention of the LPS-induced upregulation of TLR4, as was suggested by dietary administration of a flavonoid-rich supplement [29], and/or ii) a stimulation of TLR4 degradation, as was shown to occur with the addition of epigallocatechin gallate to LPS-treated adipocytes [35]. In addition, the observed positive effects associated with (−)-epicatechin supplementation can also be related to the regulation of the LPS-mediated TLR4 activation by: i) blocking the access to TLR4, as was shown for oligomerized (−)-epicatechin inhibiting the binding of LPS in HEK293 cells [36]; ii) inhibiting the capping of lipids rafts, as was shown for quercetin and luteolin in macrophages stimulated with LPS [37]; and iii) inhibiting TLR4 dimerization, as was shown for the flavonoid isoliquiritigenin, in Ba/F3 cells [38].…”

Section: Discussionmentioning

confidence: 94%

LPS-induced renal inflammation is prevented by (−)‐epicatechin in rats

et al. 2017

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This work investigated the capacity of (−)-epicatechin to prevent the renal damage induced by LPS administration in rats. Male Sprague Dawley rats were fed for 4 days a diet without or with supplementation with (−)-epicatechin (80 mg/kg BW/d), and subsequently i.p. injected with lipopolysaccharide (LPS). Six hours after injection, LPS-treated rats exhibited increased plasma creatinine and urea levels as indicators of impaired renal function. The renal cortex of the LPS-treated rats showed: i) increased expression of inflammatory molecules (TNF-α, iNOS and IL-6); ii) activation of several steps of NF-κB pathway; iii) overexpression of TLR4, and iv) higher superoxide anion production and lipid peroxidation index in association with increased levels of gp91phox and p47phox (NOX2) and NOX4. Pretreatment with dietary (−)-epicatechin prevented the adverse effects of LPS challenge essentially by inhibiting TLR4 upregulation and NOX activation and the consequent downstream events, e.g. NF-kB activation.

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“…The disruption of TLR4.MD-2 heterodimer by formation of covalent adducts with solvent-exposed MD-2 and/or TLR4 cysteines has been proposed as the main mechanism of action of 13 41 (isoliquiritigenin), 6-shoagol, 42 caffeic acid phenetyl ester 14 (CAPE) 43 and cinnamaldehyde. 44 Despite the presence of the same α, β-unsaturated carbonyl functionality, curcumin does not seem to form a covalent bond with MD-2, 45 in contrast with a previously suggested mechanism of action.…”

Section: Natural Trl4 Modulatorsmentioning

confidence: 99%

Toll-like Receptor 4 (TLR4) Modulation by Synthetic and Natural Compounds: An Update

2013

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Toll-like receptor 4 (TLR4), together with MD-2, binds bacterial endotoxins (E) with high affinity, triggering formation of the activated homodimer (E-MD-2-TLR4)2. Activated TLR4 induces intracellular signaling leading to activation of transcription factors that result in cytokine and chemokine production and initiation of inflammatory and immune responses. TLR4 also responds to endogenous ligands called danger associated molecular patterns (DAMPs). Increased sensitivity to infection and a variety of immune pathologies have been associated with either too little or too much TLR4 activation. We review here the molecular mechanisms of TLR4 activation (agonism) or inhibition (antagonism) by small organic molecules of both natural and synthetic origin. The role of co-receptors MD-2 and CD14 in the TLR4 modulation process is also discussed. Recent achievements in the field of chemical TLR4 modulation are reviewed, with special focus on non-classical TLR4 ligands with a chemical structure different from lipid A.

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Suppression of homodimerization of toll-like receptor 4 by isoliquiritigenin

Cited by 39 publications

References 30 publications

TLRs as pharmacological targets for plant-derived compounds in infectious and inflammatory diseases

TLRs as pharmacological targets for plant-derived compounds in infectious and inflammatory diseases

LPS-induced renal inflammation is prevented by (−)‐epicatechin in rats

Toll-like Receptor 4 (TLR4) Modulation by Synthetic and Natural Compounds: An Update

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