Bilirubin inhibits the up-regulation of inducible nitric oxide synthase by scavenging reactive oxygen species generated by the toll-like receptor 4-dependent activation of NADPH oxidase
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Bilirubin blocks TLR4 signaling by scavenging NADPH oxidase-derived reactive oxygen species.

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Bilirubin specifically inhibits the TRIF-dependent TLR4 signaling pathway.

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LPS activation of inducible nitric oxide synthase is mediated by HIF-1α.

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Macrophages exhibit reciprocal regulation of HIF-1α and aryl hydrocarbon receptor pathways.

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Potential mechanisms underlying the anti-inflammatory effects of bilirubin are delineated.

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