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More articles cited ChemFaces products.
Biol Pharm Bull. 2018;41(1):65-72.Mol Immunol. 2016 Oct;78:121-132.Mol Med Rep.2015 Sep 21PLoS One. 2017 Mar 9;Int J Mol Med.2015 Dec 28.
J Sep Sci.2018 Jan 23.Front Pharmacol. 2017 Sep 29;Chem Biol Interact.2018 Mar 1;Appl Microbiol Biotechnol. 2015 Dec 21. Fitoterapia.2015 Jan;100:179-86.
PhytomedicineFeb. 11. 2016Molecules. 2017 Dec 4;Inflammation.2015 Feb;38(1):445-55. Acta Physiologiae PlantarumJanuary 2016, 38:7
Our products had been exported to the following research institutions and universities, And still growing.
Universidade da Beira Interior (Germany)Julius Kühn-Institut (Germany)University of Wollongong (Australia)National Chung Hsing University (Taiwan)
University of Mysore (India)Georgia Institute of Technology (USA)Medizinische Universit?t Wien (Austria)Technical University of Denmark (Denmark)
S.N.D.T. Women's University (India)Amity University (India)Sanford Burnham Prebys Medical D... (USA)
||Artemetin has anti-inflammatory, antioxidant and antiapoptotic activities, it protects endothelial function through the activation of ERK1/2 and Akt. Intravenous injection of Artemetin (0.75 mg/kg) significantly reduces the hypertensive response to angiotensin I while increases the average length of bradykinin-induced hypotension.|
||NO | Estrogen receptor | PKA | NOS | Akt | ERK | p38MAPK | AChR | Progestogen receptor|
|Phytother Res. 2015 May 29. |
|Effects of Artemetin on Nitric Oxide Release and Protection against Peroxidative Injuries in Porcine Coronary Artery Endothelial Cells.[Pubmed: 26032176]|
|Artemetin is one of the main components of Achillea millefolium L. and Artemisia absinthium, which have long been used for the treatment of various diseases. To date, however, available information about protective effects of their extracts on the cardiovascular system is scarce. |
METHODS AND RESULTS:
Therefore, we planned to analyze the effects of Artemetin on nitric oxide (NO) release and the protection exerted against oxidation in porcine aortic endothelial (PAE) cells. In PAE, we examined the modulation of NO release caused by Artemetin and the involvement of muscarinic receptors, β2-adrenoreceptors, estrogenic receptors (ER), protein-kinase A, phospholipase-C, endothelial-NO-synthase (eNOS), Akt, extracellular-signal-regulated kinases 1/2 (ERK1/2) and p38 mitogen activated protein kinase (p38 MAPK). Moreover, in cells treated with hydrogen peroxide, the effects of Artemetin were examined on cell survival, glutathione (GSH) levels, apoptosis, mitochondrial membrane potential and transition pore opening. Artemetin increased eNOS-dependent NO production by the involvement of muscarinic receptors, β2-adrenoreceptors, ER and all the aforementioned kinases. Furthermore, Artemetin improved cell viability in PAE that were subjected to peroxidation by counteracting GSH depletion and apoptosis and through the modulation of mitochondrial function.
In conclusion, Artemetin protected endothelial function by acting as antioxidant and antiapoptotic agent and through the activation of ERK1/2 and Akt.
|Planta Med. 1990 Feb;56(1):36-40. |
|Anti-inflammatory activity and sub-acute toxicity of artemetin.[Pubmed: 2356241]|
|The 5-hydroxy-3,6,7,3',4'-pentamethoxyflavone (Artemetin) from Cordia verbenacea DC (Boraginaceae) showed marked anti-inflammatory activity using various experimental models in rats.
METHODS AND RESULTS:
Artemetin significantly inhibited carrageenin-induced paw edema following oral doses from 30.4 to 153.9 mg.kg-1. The doses of 102.6 and 153.9 mg.kg-1 showed an inhibitory effect similar to that of 50.0 mg.kg-1 of calcium phenylbutazone. The ED50 value of Artemetin in rats was estimated to be 67.07 mg.kg-1. Repeated administration of Artemetin at doses of 67.07 mg.kg-1 for a 6-day period reduced granuloma formation with a response comparable to that of 20.0 mg.kg-1 of calcium phenylbutazone. This same dose of Artemetin also reduced the vascular permeability to intracutaneous histamine. Sub-acute toxicological experiments indicated a very low toxicity.
||The herbs of Achillea millefolium L.
||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
||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
||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.
Recent ChemFaces New Products and Compounds
Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals
Cell. 2018 Jan 11;172(1-2):249-261.e12. doi: 10.1016/j.cell.2017.12.019.PMID: 29328914
Mol Cell. 2017 Nov 16;68(4):673-685.e6. doi: 10.1016/j.molcel.2017.10.022.PMID: 29149595
Scientific Reports 2017 Dec 11;7(1):17332.doi: 10.1038/s41598-017-17427-6.PMID: 29230013
Molecules. 2017 Oct 27;22(11). pii: E1829.doi: 10.3390/molecules22111829.PMID: 29077044
J Cell Biochem. 2018 Feb;119(2):2231-2239.doi: 10.1002/jcb.26385. PMID: 28857247
Phytomedicine. 2018 Feb 1;40:37-47. doi:10.1016/j.phymed.2017.12.030PMID: 29496173
Calculate Dilution Ratios(Only for Reference)
* Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
|Phytomedicine. 2011 Jul 15;18(10):819-25. |
|Hypotensive mechanism of the extracts and artemetin isolated from Achillea millefolium L. (Asteraceae) in rats.[Pubmed: 21420289 ]|
|Traditional uses of Achillea millefolium L. (Asteraceae) include the treatment of cardiovascular diseases.
METHODS AND RESULTS:
In the present study, we used anesthetized rats to assess the hypotensive effect of a hydroethanolic extract (HEAM), and its dichloromethane (DCM), ethyl acetate (EA), butanolic (BT), and dichloromethane-2 (DCM-2) fractions, besides the flavonoid Artemetin, isolated from A. millefolium. The oral administration of HEAM (100-300 mg/kg), DCM (20mg/kg), DCM-2 (10-30 mg/kg), but not EA (10 mg/kg) and BT (50 mg/kg) fractions significantly reduced the mean arterial pressure (MAP) of normotensive rats. The phytochemical analysis by NMR (1)H of DCM and DCM-2 fractions revealed high amounts of Artemetin, that was isolated and administered by either oral (1.5 mg/kg) or intravenous (0.15-1.5 mg/kg) routes in rats. This flavonoid was able to dose-dependently reduce the MAP, up to 11.47 ± 1.5 mmHg (1.5 mg/kg, i.v.). To investigate if Artemetin-induced hypotension was related to angiotensin-converting enzyme inhibition, we evaluated the influence of this flavonoid on the vascular effects of both angiotensin I and bradykinin. Intravenous injection of Artemetin (0.75 mg/kg) significantly reduced the hypertensive response to angiotensin I while increased the average length of bradykinin-induced hypotension. Artemetin (1.5 mg/kg, p.o.) was also able to reduce plasma (about 37%) and vascular (up to 63%) ACE activity in vitro, compared to control group. On the other hand, Artemetin did not change angiotensin II-induced hypertension.
Our study is the first showing the hypotensive effects induced by the extract and fractions obtained from A. millefollium. In addition, our results disclosed that this effect may be, at least in part, associated with high levels of Artemetin and its ability to decrease angiotensin II generation in vivo, by ACE inhibition.