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Matches in Nanopublications for { ?s ?p "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." ?g. }

• _4 value "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." provenance.
• _4 value "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." provenance.