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tscript(complex(SCOMP:"Nfkb Complex")) -> r(HGNC:RETN)
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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
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BEL Framework Large Corpus Document
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Rosiglitazone has marked anti-inflammatory effects on macrophages [31]. This led us to examine the effect of aspirin, an anti-inflammatory compound that targets IkB kinase and has insulin-sensitizing effects [32]. Remarkably, aspirin dramatically decreased endotoxin-induced resistin expression in a dose-dependent manner (Figure 4C). Both aspirin (via IkB kinase) and rosiglitazone (via PPARg) inhibit NF-kB [31,32], which is activated by LPS. Indeed, treatment of the macrophages with the proteasome inhibitor MG132, which prevents NF-kB activation [33], abrogated endotoxin-induced activation of resistin expression (data not shown). Moreover, treatment of the macrophages with SN50, a cell-permeable peptide that specifically prevents activation of NF-kB by inhibiting its nuclear translocation [34], nearly abolished endotoxin-induced activation of resistin expression (Figure 4D). Thus, activation of NF-kB is required for LPS induction of resistin in human macrophages.
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Selventa
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