The effect of piceatannol on lipopolysaccharide (LPS)-induced nitric oxide (NO) production was examined. Piceatannol significantly inhibited NO production in LPS-stimulated RAW 264.7 cells. The inhibition was due to the reduced expression of an inducible isoform of NO synthase (iNOS). The inhibitory effect of piceatannol was mediated by down-regulation of LPS-induced nuclear factor (NF)-κB activation, but not by its cytotoxic action. Piceatannol inhibited IκB kinase (IKK)-α and β phosphorylation, and subsequently IκB-α phosphorylation in LPS-stimulated RAW 264.7 cells. On the other hand, piceatannol did not affect activation of mitogen-activated protein (MAP) kinases including extracellular signal regulated kinase 1/2 (Erk1/2), p38 and stress-activated protein kinase/c-Jun NH2-terminal kinase (SAPK/JNK). Piceatannol inhibited the phosphorylation of Akt and Raf-1 molecules, which regulated the activation of IKK-α and β phosphorylation. The detailed mechanism of the inhibition of LPS-induced NO production by piceatannol is discussed.
|Number of pages||8|
|Journal||MICROBIOLOGY and IMMUNOLOGY|
|Publication status||Published - 2004|
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