|Source:||The herb of Carex humilis Leyss.|
|Biological Activity or Inhibitors:||1. Alpha-viniferin has anti-inflammatory, anti-oxidant, anti-arthritis, and anti-tumor activities.
2. 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.
3. Alpha-Viniferin has anti-inflammatory activity, down-regulating STAT-1-inducible inflammatory genes via inhibiting ERK-mediated STAT-1 activation in IFN-gamma-stimulated macrophages.
4. 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.
5. Alpha-viniferin is a prostaglandin H2 synthase inhibitor, the inhibitory potency of (+)-alpha-viniferin is about 3- to 4-fold stronger than that of resveratrol on cyclooxygenase activity of prostaglandin H2 synthase partially purified from sheep seminal vesicles.
|Solvent:||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: email@example.com
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||1.4734 mL||7.367 mL||14.7341 mL||29.4681 mL||36.8351 mL|
|5 mM||0.2947 mL||1.4734 mL||2.9468 mL||5.8936 mL||7.367 mL|
|10 mM||0.1473 mL||0.7367 mL||1.4734 mL||2.9468 mL||3.6835 mL|
|50 mM||0.0295 mL||0.1473 mL||0.2947 mL||0.5894 mL||0.7367 mL|
|100 mM||0.0147 mL||0.0737 mL||0.1473 mL||0.2947 mL||0.3684 mL|
Food Chem Toxicol. 2014 Jul;69:276-80.
|Potent inhibitory effect of alpha-viniferin on human cytochrome P450.[Pubmed: 24769006]|
|alpha-Viniferin isolated from Caragana chamlagu is a trimer of resveratrol, and has several biological activities, which include anti-inflammatory, anti-oxidant, anti-arthritis, and anti-tumor activities. Herb-drug interactions are the source of the most harmful complications in patients coadministered herbal and modern medicines, and are caused by modulation of the activities of drug metabolizing enzymes. Here, the authors investigated the inhibitory effects of alpha-Viniferin on the activities of 9 human cytochrome P450 (CYP) isoforms using a cocktail of probe substrates and LC-MS/MS in pooled human liver microsomes (HLMs). alpha-Viniferin strongly inhibited 7 of the 9 CYP isoforms (except CYP2A6 and CYP2E1). Furthermore, alpha-Viniferin strongly inhibited CYP2C19-mediated omeprazole 5-hydroxylation and CYP3A4-catalyzed midazolam 1-hydroxylation with IC50 values of 0.93 and 1.2 μM, respectively. alpha-Viniferin strongly inhibited the activities of these two CYPs dose dependently, but not time-dependently. Lineweaver-Burk plots and secondary plots indicated a typical pattern of mix-mode inhibition for CYP2C19 and 3A4. This is the first investigation conducted on the inhibitory effect of alpha-Viniferin on CYP2C19 and 3A4 in HLMs to predict a potential herb-drug interaction.|
Cell Immunol. 2014 Jul;290(1):21-9.
|Anti-inflammatory mechanism of α-viniferin regulates lipopolysaccharide-induced release of proinflammatory mediators in BV2 microglial cells.[Pubmed: 24859013]|
|alpha-Viniferin is an oligostilbene of trimeric resveratrol and has anticancer activity; however, the molecular mechanism underlying the anti-inflammatory effects of alpha-Viniferin has not been completely elucidated thus far. Therefore, we determined the mechanism by which alpha-Viniferin regulates lipopolysaccharide (LPS)-induced expression of proinflammatory mediators in BV2 microglial cells. Treatment with alpha-Viniferin isolated from Clematis mandshurica decreased LPS-induced production of nitric oxide (NO) and prostaglandin E2 (PGE2). alpha-Viniferin also downregulated the LPS-induced expression of proinflammatory genes such as iNOS and COX-2 by suppressing the activity of nuclear factor kappa B (NF-κB) via dephosphorylation of Akt/PI3K. Treatment with a specific NF-κB inhibitor, pyrrolidine dithiocarbamate (PDTC), indirectly showed that NF-κB is a crucial transcription factor for expression of these genes in the early stage of inflammation. Additionally, our results indicated that alpha-Viniferin suppresses NO and PGE2 production in the late stage of inflammation through induction of heme oxygenase-1 (HO-1) regulated by nuclear factor erythroid 2-related factor (Nrf2). Taken together, our data indicate that alpha-Viniferin suppresses the expression of proinflammatory genes iNOS and COX-2 in the early stage of inflammation by inhibiting the Akt/PI3K-dependent NF-κB activation and inhibits the production of proinflammatory mediators NO and PGE2 in the late stage by stimulating Nrf2-mediated HO-1 signaling pathway in LPS-stimulated BV2 microglial cells. These results suggest that alpha-Viniferin may be a potential candidate to regulate LPS-induced inflammation.|
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. 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. 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.|
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. 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. In conclusion, alpha-Viniferin suppressed arthritic inflammation and bony change in rats.|
Planta Med. 1998 Apr;64(3):204-7.
|Alpha-viniferin: a prostaglandin H2 synthase inhibitor from root of Carex humilis.[Pubmed: 9581514]|
|An inhibitor on cyclooxygenase activity of prostaglandin H2 synthase was purified from the root of Carex humilis Leyss (Cyperaceae) by a variety of column chromatographic methods. As a result of the structure analysis by FAB-mass, 1H-NMR, and 13C-NMR spectral data, the active compound was identified as (+)-alpha-Viniferin, an oligomeric stilbene characterized originally from Caragana chamlagu Lamarck (Leguminosae). (+)-alpha-Viniferin exhibited a dose-dependent inhibition on cyclooxygenase activity, where 50% of inhibition (IC50) was shown at a final concentration of about 7 microM. Resveratrol, a putative building block of oligomeric stilbenes, also inhibited the cyclooxygenase activity. The inhibitory potency of (+)-alpha-Viniferin was about 3- to 4-fold stronger than that of resveratrol on cyclooxygenase activity of prostaglandin H2 synthase partially purified from sheep seminal vesicles.|