Piceatannol Prevents Lipopolysaccharide (LPS)‐Induced Nitric Oxide (NO) Production and Nuclear Factor (NF)‐κB Activation by Inhibiting IκB Kinase (IKK)
2004; Wiley; Volume: 48; Issue: 10 Linguagem: Inglês
10.1111/j.1348-0421.2004.tb03598.x
ISSN1348-0421
AutoresShamima Islam, Ferdaus Hassan, Mya Mya Mu, Hiroyasu Ito, Naoki Koide, Isamu Mori, Tomoaki Yoshida, Takashi Yokochi,
Tópico(s)Bioactive natural compounds
ResumoAbstract 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 I K B‐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.
Referência(s)