alpha-Viniferin Inhibitor

Solid. Powder

98.00%

Store at -20 degree C for 3 years powder
-80 degree C for 2 years in solvent

678.7

<1mg/ml refers to the product slightly soluble or insoluble

C42H30O9

[H][C@]12[C@@H](Oc3cc(O)cc(c13)[C@]1([H])[C@H](Oc3cc(O)cc(c13)[C@@]1([H])[C@@H](Oc3cc(O)cc2c13)c1ccc(O)cc1)c1ccc(O)cc1)c1ccc(O)cc1

62218-13-7

P450
NO Synthase
PGE

Alpha-Viniferin at 3 - 10microM dose-dependently inhibited interferon (IFN)-gamma-induced Ser(727) phosphorylation of the signal transducer and activation of transcription-1 (STAT-1), a pivotal transcription factor controlling IFN-gamma-targeted genes, in RAW 264.7 macrophages, and also IFN-gamma-induced activation of the extracellular signal-regulated kinase (ERK)-1, a protein kinase upstream of the Ser(727) phosphorylation of STAT-1. However, alpha-Viniferin, only at a higher concentration of 10microM, inhibited Janus kinase 2-mediated Tyr(701) phosphorylation of STAT-1 in the cells. To understand STAT-1-dependent inflammatory responses, we quantified nitric oxide (NO) or chemokines. Alpha-Viniferin at 3-10muM dose-dependently inhibited IFN-gamma-induced production of NO, IFN-gamma-inducible protein-10 (IP-10), or the monokine induced by IFN-gamma (MIG) in RAW 264.7 cells and also that of NO in primary macrophages-derived from C57BL/6 mice. Furthermore, alpha-Viniferin diminished IFN-gamma-induced protein levels of inducible NO synthase (iNOS), attenuated mRNA levels of iNOS, IP-10, or MIG as well as inhibited promoter activity of the iNOS gene.

Metabolism; P450; Immunology/Inflammation; GPCR/G Protein