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KMID : 1134820120410091226
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Journal of the Korean Society of Food Science and Nutrition
2012 Volume.41 No. 9 p.1226 ~ p.1234
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Mechanism Underlying the Anti-Inflammatory Action of Piceatannol Induced by Lipopolysaccharide
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Cho Han-Jin
Shim Jae-Hoon
So Hong-Seob
Yoon Jung-Han
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Abstract
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3,4,3',5'-Tetrahydroxy-trans-stilbene (piceatannol) is a derivative of resveratrol with a variety of biological activities, including anti-inflammatory, anti-proliferative, and anti-cancer activities. We assessed the mechanisms by which piceatannol inhibits inflammatory responses using lipopolysaccharide (LPS)-treated Raw264.7 murine macrophages. Piceatannol (0～10 μmol/L) decreased LPS-induced release of nitric oxide, tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, and inhibited LPS-induced protein expression of inducible nitric oxide synthase (iNOS). Activation of nuclear factor-kappaB (NF-κB), activator protein (AP)-1, and signal transducer and activator of transcription 3 (STAT3) are crucial steps during an inflammatory response. Piceatannol prevented LPS-induced degradation of inhibitor of κB (IκB), translocation of p65 to the nucleus, and phosphorylation of stress-activated protein kinase/c-Jun NH2-terminal kinase (SAPK/JNK). Additionally, piceatannol inhibited LPS-induced phosphorylation of STAT3 and IL-6-induced translocation of STAT3 to the nucleus. Furthermore, piceatannol increased the protein and mRNA levels of hemeoxygenase (HO)-1, the rate-limiting enzyme of heme catabolism that plays a critical role in mediating antioxidant and anti-inflammatory effects. Piceatannol further induced antioxidant response elements (ARE)-driven luciferase activity in Raw264.7 cells transfected with an ARE-luciferase reporter construct containing the enhancer 2 and minimal promoter region of HO-1. These results suggest that piceatannol exerts anti-inflammatory effects via the down-regulation of iNOS expression and up-regulation of HO-1 expression.
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KEYWORD
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piceatannol, iNOS, NF-κB, STAT3, HO-1
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