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More articles cited ChemFaces products.
J of Advanced Scientific R....2020...Acta Agriculturae Scandinavica...2015...Phytomedicine.2021, 83:153483. Chinese Journal of Hospital Pharm...2020...Mol Pharm.2017, 14(9):3164-3177J Nat Med.2020, 74(1):65-75Phytomedicine.2017, 24:77-86Front Pharmacol.2018, 9:236
Universidade Estadual Paulista...2017...J Ethnopharmacol.2019, 228:132-141Int Immunopharmacol.2020, 90:107268.J Cancer.2019, 10(23):5843-5851Appl. Sci. 2021, 11(22),10569Toxicol In Vitro.2018, 52:94-105The Journal of Phytopharmacology...2020...Phytother Res.2019, 33(3):676-689
Genes Genomics.2020, 10.1007Evid Based Complement Alternat Me...2021...Journal of Third Military Medical...2019...Plants (Basel).2020, 9(11):1422.Br J Pharmacol.2020, 10.1111Cell Mol Biol(Noisy-le-grand)...2019...Antioxidants (Basel).2021, 10(3):379.
Our products had been exported to the following research institutions and universities, And still growing.
Rio de Janeiro State University (Brazil)University of Canterbury (New Zealand)Johannes Gutenberg University M... (Germany)Mahidol University (Thailand)
Universidade do Porto (Portugal)Tokyo Woman's Christian University (Japan)University of Maryland (USA)Univerzita Karlova v Praze (Czech Republic)
The University of Newcastle (Australia)Northeast Normal University Cha... (China)Martin Luther University of Hal... (Germany)
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Korean Journal of Pharmacognosy2018, 49(4):349-361Saf Health Work.2019, 10(2):196-204PLoS One.2017, 12(3):e0173585Plant Cell Tiss Org2017, 479-486Chin J Pharm Anal.2019, 39(7):1217-1228Molecules.2021, 26(6):1738. Toxicol Res.2019, 35(4):371-387J Ethnopharmacol.2017, 197:157-164European Journal of Integrative Medicine2018, 20:165-172J Ethnopharmacol.2020, 249:112381
Related Screening Libraries
||alpha-Asarone has antioxidant activity, it effectively reversed MDR by inhibiting P-gp function and expression. alpha-Asarone protects against Ang II-mediated damage of endothelial cells and may be developed to prevent injury to cardiovascular tissues. Alpha-asarone congeners as hypolipidemic agents, they appeared to be promising for the treatment of human hyperlipidaemia and thrombotic diseases.Alpha-asarone also attenuates depression-like behavior in nicotine-withdrawn mice.
||P-gp | ROS | NO | eNOS | LDL | SOD | GPx | pCREB | BDNF|
| BIOTECHNOLOGY LETTERS, 2014, 36(4):685. |
|Reversing P-glycoprotein-mediated multidrug resistance in vitro by α-asarone and β-asarone, bioactive cis–trans isomers from Acorus tatarinowii.[Reference: WebLink]|
|P-Glycoprotein (P-gp), an ATP-binding cassette transporter, plays an important role in multidrug resistance (MDR). |
METHODS AND RESULTS:
and β-asarone, bioactive cis–trans isomers found in Acorus tatarinowii Schott, were tested for their potential ability to modulate the expression and function of P-gp in Caco-2 cells. MTT assays revealed that both alpha-Asarone and β-asarone significantly enhanced the vincristine-induced cytotoxicity to cells. β-Asarone was the most potent. Flow cytometry showed that alpha-Asarone
and β-asarone increased Rhodamine 123 (Rh123) uptake and inhibited Rh123 efflux in Caco-2 cells in a concentration-dependent manner. Furthermore, P-gp expression and P-gp mRNA in cells were decreased by exposure to alpha-Asarone and β-asarone. In addition, β-asarone increased the inhibition of P-gp activity in cells more than α-asarone.
Thus, alpha-Asarone and β-asarone effectively reversed MDR by inhibiting P-gp function and expression.
|Evidence-Based Complementary and Alternative Medicine, 2014, 2014:1-7. |
|Alpha-Asarone Protects Endothelial Cells from Injury by Angiotensin II.[Pubmed: 24757494 ]|
|alpha-Asarone is the major therapeutical constituent of Acorus tatarinowii Schott. |
METHODS AND RESULTS:
In this study, the potential protective effects of alpha-Asarone
against endothelial cell injury induced by angiotensin II were investigated in vitro. The EA.hy926 cell line derived from human umbilical vein endothelial cells was pretreated with alpha-Asarone
(10, 50, 100 µmol/L) for 1 h, followed by coincubation with Ang II (0.1 µmol/L) for 24 h. Intracellular nitric oxide (NO) and reactive oxygen species (ROS) were detected by fluorescent dyes, and phosphorylation of endothelial nitric oxide synthase (eNOS) at Ser1177 was determined by Western blotting. alpha-Asarone
dose-dependently mitigated the Ang II-induced intracellular NO reduction (P < 0.01 versus model) and ROS production (P < 0.01 versus model). Furthermore, eNOS phosphorylation (Ser1177) by acetylcholine was significantly inhibited by Ang II, while pretreatment for 1 h with alpha-Asarone partially prevented this effect (P < 0.05 versus model). Additionally, cell viability determined by the MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay (105~114.5% versus control, P > 0.05) was not affected after 24 h of incubation with α-asarone at 1–100 µmol/L.
Therefore, alpha-Asarone protects against Ang II-mediated damage of endothelial cells and may be developed to prevent injury to cardiovascular tissues.
|Journal of Pharmacy & Pharmacology, 2010, 58(10):1343-1349. |
|Hypolipidaemic and antiplatelet activity of phenoxyacetic acid derivatives related to α-asarone.[Reference: WebLink]|
|The phenoxyacetic acid derivatives 1-6 [2-methoxy-4-(2-propenyl)phenoxyacetic acid (1); 2-methoxy-5-nitro-4-(2-propenyl)phenoxyacetic acid (2); methyl 2-methoxy-4-(2-propenyl)phenoxyacetate (3); ethyl 2-methoxy-4-(2-propenyl)phenoxyacetate (4); methyl 2-methoxy-5-nitro-4-(2-propenyl)phenoxyacetate (5); ethyl 2-methoxy-5-nitro-4-(2-propenyl)phenoxyacetate (6)] related to alpha-Asarone have been reported previously as hypolipidaemic agents in diet-induced hyperlipidaemic mice. We have aimed to expand the pharmacological profile of these derivatives by investigating their hypolipidaemic activity in rats and mice under different experimental conditions. The antiplatelet activity was tested also in-vitro from blood derived from consenting healthy volunteers. |
METHODS AND RESULTS:
In normolipidaemic rats, compounds 2, 3 and 5 at oral doses of 40 and 80 mg kg(-1) significantly decreased total cholesterol and LDL-cholesterol levels. Moreover, analogues 3 and 5 administered to hypercholesterolaemic rats at the same doses for seven days also produced a reduction in the content of these same lipoproteins. In neither case were the high-density lipoprotein cholesterol and triglyceride concentrations affected. However, practically all tested compounds were found to be hypocholesterolaemic agents, and were shown to effectively lower low-density lipoprotein cholesterol and triglyceride levels in Triton-induced hyperlipidaemic mice at oral doses of 50 and 100 mg kg(-1).
In all tests, all animals appeared to be healthy throughout the experimental period in their therapeutic ranges. Triton-induced hypercholesterolaemic mice appeared to be a desirable model for this class of hypolipidaemic drugs. On the other hand, compounds 1, 2, 4 and 5 significantly inhibited ADP-induced aggregation in-vitro. These findings indicated that all of these compounds appeared to be promising for the treatment of human hyperlipidaemia and thrombotic diseases.
||The seeds of Daucus carota
||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: firstname.lastname@example.org
||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.
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.IF=36.216(2019)PMID: 29328914
Cell Metab. 2020 Mar 3;31(3):534-548.e5. doi: 10.1016/j.cmet.2020.01.002.IF=22.415(2019)PMID: 32004475
Mol Cell. 2017 Nov 16;68(4):673-685.e6. doi: 10.1016/j.molcel.2017.10.022.IF=14.548(2019)PMID: 29149595
ACS Nano. 2018 Apr 24;12(4): 3385-3396. doi: 10.1021/acsnano.7b08969.IF=13.903(2019)PMID: 29553709
Nature Plants. 2016 Dec 22;3: 16206. doi: 10.1038/nplants.2016.205.IF=13.297(2019)PMID: 28005066
Sci Adv. 2018 Oct 24;4(10): eaat6994. doi: 10.1126/sciadv.aat6994.IF=12.804(2019)PMID: 30417089
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* 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.
|Pharmacological Research, 2005, 52(6):467-474. |
|Antioxidant property of alpha-asarone against noise-stress-induced changes in different regions of rat brain.[Reference: WebLink]|
|Free radicals and other reactive species are considered to be an important causative factor in the development of neurodegenerative diseases. Recent reports have indicated that exposure to loud noise generates excess oxygen free radicals (OFR) in the brain.
Antioxidant properties of medicinal plants are attracting more and more research in medicine, to counteract OFR and to minimize the neurodegenerative processes. |
METHODS AND RESULTS:
The drug alpha-Asarone (3, 6 and 9 mg kg(-1) body weight, i.p., for 30 days), one of the active principle components of Acorus calamus Linn., was administered intraperitoneally 1/2 h before the animals were exposed to noise-stress (100 dB for 4 h d(-1), for 30 days). We investigated whether 30 days exposure of noise can produce an oxidative stress. Further, if yes then, could alpha-Asarone counteract the stress. This was verified by measuring the activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), levels of reduced glutathione (GSH), Vitamin C, Vitamin E, protein thiols and lipid peroxidation (LPO) in different regions of the rat brain. All the three doses of alpha-Asarone had an effectively protective role by normalizing the increased SOD and LPO, decreased CAT, GPx, GSH, Vitamins C and E and protein thiols due to noise exposure. Thus, action of alpha-Asarone against noise-stress may be due its antioxidant property.
Our data proved that antioxidant property of alpha-Asarone against noise-stress induced changes in the rat brain. Further, more clinical studies are required to investigate effectiveness of the alpha-Asarone in noisy environment in human subjects.
|European Journal of Pharmacology, 2017:S001429991730674X. |
|Alpha-asarone attenuates depression-like behavior in nicotine-withdrawn mice: Evidence for the modulation of hippocampal pCREB levels during nicotine-withdrawal.[Pubmed: 29042206]|
|In the present study, the effect alpha-Asarone on nicotine withdrawal-induced depression-like behavior in mice was investigated.|
METHODS AND RESULTS:
In this study, mice were exposed to drinking water or nicotine solution (10–200 µg/ml) as a source of drinking for forty days. During this period, daily fluid consumption, food intake and body weight were recorded. The serum cotinine level was estimated before nicotine withdrawal. Naïve mice or nicotine-withdrawn mice were treated with alpha-Asarone
(5, 10 and 20 mg/kg, i.p.) or bupropion (10 mg/kg, i.p.) for eight consecutive days and the forced swim test (FST) or locomotor activity test was conducted. In addition, the effect of alpha-Asarone
or bupropion on the hippocampal pCREB, CREB and BDNF levels during nicotine-withdrawal were measured. Results indicated that alpha-Asarone (5, 10 and 20 mg/kg, i.p.) or bupropion (10 mg/kg, i.p.) pretreatment did not significantly alter the immobility time in the FST or spontaneous locomotor activity in naïve mice. However, the immobility time of nicotine-withdrawn mice was significantly attenuated with alpha-Asarone (5, 10 and 20 mg/kg, i.p.) or bupropion (10 mg/kg, i.p.) pretreatment in the FST. Besides, alpha-Asarone
(5, 10 and 20 mg/kg, i.p.) or bupropion (10 mg/kg, i.p.) pretreatment significantly attenuated the hippocampal pCREB levels in nicotine-withdrawn mice.
Overall, the present results indicate that alpha-Asarone
treatment attenuated the depression-like behavior through the modulation of hippocampal pCREB levels during nicotine-withdrawal in mice.