IndraLab

Statements



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"In mouse gouty arthritis models, oral administration of CAPE suppressed MSU crystals induced caspase-1 activation and IL-1beta production in the air pouch exudates and the foot tissues, correlating with attenuation of inflammatory symptoms."

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"In primary mouse macrophages, caffeic acid phenethyl ester (CAPE) blocked caspase-1 activation and IL-1beta production induced by MSU crystals, showing that CAPE suppresses NLRP3 inflammasome activation."

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"In primary mouse macrophages, caffeic acid phenethyl ester (CAPE) blocked caspase-1 activation and IL-1beta production induced by MSU crystals, showing that CAPE suppresses NLRP3 inflammasome activation."

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"CAPE suppressed ATP induced cleavage of pro-caspase-1 and pro-IL-1beta to caspase-1 (p10) and IL-1beta in BMDMs (XREF_SUPPLEMENTARY) and reduced ATP induced secretion of IL-1beta and IL-18 (XREF_SUPPLEMENTARY)."

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"CAPE did not directly bind to NLRP3 PYD, nor inhibited caspase-1 enzyme activity."

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"An in vitro caspase-1 enzyme activity assay confirmed that CAPE did not directly inhibit caspase-1 activity (XREF_FIG)."

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"Oral administration of CAPE prevented the cleavage of pro-caspase-1 to caspase-1 (p10) and of pro-IL-1beta to IL-1beta in foot tissue injected with MSU crystals (XREF_FIG)."

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"In a mouse gouty arthritis model, oral administration of CAPE inhibited MSU crystal induced caspase-1 activation and IL-1beta production in air pouch exudate and foot tissue thus attenuating inflammatory symptoms."

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"CAPE inhibited MSU crystal induced cleavage of pro-caspase-1 and pro-IL-1beta, to caspase-1 (p10) and IL-1beta, respectively, in the cellular supernatants (XREF_FIG)."

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"In vivo, CAPE inhibited the activity of iNOS and caspase-1 in the brain of mice treated with MPTP [XREF_BIBR]."