| Description: |
Alpha-viniferin is a prostaglandin H2 synthase inhibitor, which has anti-inflammatory, anti-oxidant, anti-arthritis, and anti-tumor activities. Alpha-Viniferin inhibits AChE activity is specific, reversible and noncompetitive, in a dose-dependent manner, and the IC50 values of alpha-Viniferin were 2.0 microM. Alpha-Viniferin exhibits a dose-dependent inhibition on cyclooxygenase activity, where 50% of inhibition (IC50) was shown at a final concentration of about 7 microM, it down-regulates STAT-1-inducible inflammatory genes via inhibiting ERK-mediated STAT-1 activation in IFN-gamma-stimulated macrophages. |
| Targets: |
P450 (e.g. CYP17) | NO | PGE | NOS | COX | NF-kB | Akt | PI3K | HO-1 | Nrf2 | IFN-γ | STAT | ERK | AChR |
| In vitro: |
| J Pharmacol Sci. 2010;112(4):405-14. | | alpha-Viniferin suppresses the signal transducer and activation of transcription-1 (STAT-1)-inducible inflammatory genes in interferon-gamma-stimulated macrophages.[Pubmed: 20424383] | alpha-Viniferin, an oligostilbene of trimeric resveratrol, has been reported to have anti-inflammatory potential in carrageenin-induced paw edema or adjuvant-induced arthritis in animal models. However, little is known about the molecular basis.
METHODS AND RESULTS:
In this study, alpha-Viniferin at 3 - 10 microM 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 10 microM, 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 - 10 muM 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.
CONCLUSIONS:
In conclusion, this study proposes an anti-inflammatory mechanism of alpha-Viniferin, down-regulating STAT-1-inducible inflammatory genes via inhibiting ERK-mediated STAT-1 activation in IFN-gamma-stimulated macrophages. |
|
| In vivo: |
| Am J Chin Med. 2004;32(4):521-30. | | The effects of alpha-viniferin on adjuvant-induced arthritis in rats.[Pubmed: 15481642] | This study was performed to assess the efficacy of alpha-Viniferin (Carex humilis Leyss) on adjuvant-induced arthritis in rats. Adjuvant arthritis was induced by a single subcutaneous injection of 0.1 ml complete Freund's adjuvant (CFA) containing 7.5 mg Mycobacterium butyricum suspended in 1 ml sterile paraffin oil into the right hind paw.
METHODS AND RESULTS:
Forty female Sprague-Dawley rats were injected. Righting reflex was uniformly lost and considered to be the initial point of arthritis development on day 7 after CFA injection. Rats were divided into four groups, and upon development of arthritis, tested groups were orally administered 3 or 10 mg/kg alpha-Viniferin or 10 mg/kg ketoprofen every day for 14 days. The control group was orally administered 2 ml of physiological saline solution. Bone mineral density (BMD), radiological changes and edematous volumes were measured for 35 days. alpha-Viniferin suppressed the development of inflammatory edema, and inhibited the bone destruction, noted with a decrease in BMD (p < 0.05). Hind paw edema volume, BMD and radiological changes did not differ significantly in the ketoprofen and alpha-Viniferin groups during the entire study period.
CONCLUSIONS:
In conclusion, alpha-Viniferin suppressed arthritic inflammation and bony change in rats. |
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