IndraLab

Statements


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"Here we demonstrate that the anti-inflammatory agents aspirin and sodium salicylate specifically inhibit IKK-beta activity in vitro and in vivo."

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"It has been shown that aspirin, as well as sodium salicylate, inhibits IKK-beta activity in vitro at millimolar concentration [XREF_BIBR] by binding to IKK-beta, thus, competing with ATP for the binding to the kinase, an event necessary to phosphorylate IkB [XREF_BIBR, XREF_BIBR]."

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"Recently, sodium salicylate and aspirin have been shown to inhibit activation of the transcription factor NF-kappaB by preventing IKK-beta from degradation."

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"Yuan et al. [XREF_BIBR] demonstrated that reduced signaling through the IKK-beta pathway inhibition by sodium salicylate in obese mice is accompanied by improved insulin sensitivity."

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"In the present study, we wished to test the hypothesis that sodium salicylate, which inhibits IKKbeta, prevents hepatic insulin resistance caused by short-term elevation of FFA."

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"High concentrations of sodium salicylate are known to mediate its anti-inflammatory property by inhibiting the cellular kinase IKK-beta, as opposed to working through its classical target cyclooxygenase (COXs) [XREF_BIBR]."

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"Whereas sulfasalazine was found to inhibit both IKKalpha and IKKbeta, aspirin and sodium salicylate were reported to specifically inhibit IKKbeta."

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"Indeed, IKKbeta phosphorylates Bcl-xL (XREF_FIG, top panel), and this is specific since inhibition of IKKbeta by sodium salicylate prevents this reaction, and IKKalpha does not phosphorylate Bcl-xL."

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"We hypothesized that sodium salicylate would reduce IKKbeta, leading to reduced TNFalpha and improved insulin signaling in the BBZDR and Wor obese rat model of type 2 diabetes."