• Journal of the East Asian Society of Dietary Life
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• v.21 no.5
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• pp.739-745
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• 2011

This study was performed to investigate the enrichment of resveratrol content in harvested grapes using the modulation of cell metabolism with ultra-violet (UV) irradiation. Resveratrol, a phytoalexin, is produced by stilbene synthase (STSY) from malonyl-CoA and ${\rho}$-coumaroyl-CoA. Its biosynthesis has been reported to be induced by UV and other environmental factors. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis showed that STSY Promoter 1 in grapes was very highly expressed by treatment with UV. Grapes were harvested and treated for post-harvest induction of STSY gene expression with UV, and then their resveratrol content was analyzed. UV treatment for 5 minutes provided the best condition for the induction of STSY gene expression. When harvested Gerbong and MBA grapes were treated with a prototype UV radiator, their resveratrol content was enriched upto 5 times compared with untreated grapes. These results suggest that a post-harvest UV treatment can be applied to enrich resveratrol content in grapes and add value to them.

• Journal of the Korean Society of Food Science and Nutrition
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• v.41 no.9
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• pp.1226-1234
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• 2012

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 ${\mu}mol/L$) decreased LPS-induced release of nitric oxide, tumor necrosis factor (TNF)-${\alpha}$, interleukin (IL)-6, IL-$1{\beta}$, and inhibited LPS-induced protein expression of inducible nitric oxide synthase (iNOS). Activation of nuclear factor-kappaB (NF-${\kappa}B$), 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 ${\kappa}B$ ($I{\kappa}B$), 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.