Resveratrol是一种多酚类植物抗毒素，具有抗氧化和化学预防活性。 它具有广泛的目标，包括 COX、SIRT、LOC 等。

Resveratrol is a polyphenolic phytoalexin with antioxidant and chemopreventive activities. It has a wide spectrum of targets including COX, SIRT, LOC, etc.

Resveratrol inhibits cellular events associated with tumor initiation, promotion, and progression. Resveratrol inhibited the hydroperoxidase activity of COX-1 (ED50 = 3.7 μM) [1]. Resveratrol inhibits the activity of COX-1 and COX-2 (IC50s: 1.1 μM and 1.3 μM for COX-1 and COX-2, respectively) [2]. Resveratrol inhibited TPA-induced DNA binding of NF-kB. Moreover, resveratrol reduced the levels of p65/RelA, a functionally active subunit of NF-kB in nuclear fractions prepared from TPA-treated mouse skin. Resveratrol pretreatment significantly inhibited the phosphorylation of p65-(Ser-536) induced by TPA. Resveratrol pretreatment significantly attenuated TPA-induced stimulation of IKKa and IKKb activity [3]. DNA polymerase inhibiting activity of resveratrol was found to occur at 10 μM in an SV40 viral DNA replication assay. Resveratrol inhibits DNA polymerases α and δ (IC50s: 3.3 and 5 μM, respectively) [4].

Resveratrol (RSV) treatment significantly upregulated eNOS gene expression and the levels of phosphorylated CREB in the aorta compared with the untreated control mice. Simultaneously, RSV treatment was observed to upregulate PKA activity and cGMP levels and inhibited superoxide generation in the aorta compared with untreated mice. Compared to vehicle-treated mice, chronic RSV treatment resulted in a significant improvement in endothelium-dependent vasorelaxation response to Ach. Treatment with RSV markedly attenuated the area of atherosclerotic lesions [5].

HAECs were treated with RSV in the presence of isobutylmethylxanthine (IBMX). The reaction was stopped by adding ice-cold 6% trichloroacetic acid and the supernatant fractions of the cellular lysates were extracted, dried and acetylated. Cyclic GMP levels were determined by an enzyme immunoassay kit and results standardized by protein levels [5].

Eight-week male apoE-/- mice (C57BL/6 background) were used in the study. Mice were housed in photobiologic light-exposure chambers with a 12:12-h light:dark cycle, and eat food ad libitum. Mice were randomly divided into two groups: one group receiving a high cholesterol diet (HCD, 21% fat, 19.5% casein, and 1.5% cholesterol), the other receiving HCD supplemented with RSV (200 mg/100 g diet). All mice were fed for 8 weeks. To identify the potential role of PKA, some mice were treated with PKA specific inhibitor (KT5720, 1.2 mg/kg) via intraperitoneal injection once a day at the last 4 weeks. The animal experiments were conducted according to the institutional guidelines of Guangdong Provincial People's Hospital [5].

501-36-0

C14H12O3

228.247

白藜芦醇;trans-Resveratrol;SRT 501

H2O:<1 mgml
Ethanol:<1 mgml
DMSO:42 mg/mL (184 mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years