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More articles cited ChemFaces products.
Oncology LettersJan. 25, 2018;Semyung UniversityJan. 2017;FEBS Lett.2015 Jan 2;589(1):182-7. Phytochem Anal.2016 Sep;Int J Mol Sci.2015 Jan 6;16(1):1232-51.
Biol Pharm Bull. 2018;41(1):65-72.Biochem Pharmacol. 2017 Apr 15;Sci Rep. 2017 Jun 12;J Agric Food Chem.2016 Sep 7J Chromatogr B Analyt Tec. Bio. Life Sci. 2018 Feb 17;
Jou. of Agromedicine and Med. Sci.2018;PhytomedicineFeb. 11. 2016Hum Exp Toxicol. 2016 Dec 9.J Agric Food Chem. 2017 Apr 5
Our products had been exported to the following research institutions and universities, And still growing.
National Chung Hsing University (Taiwan)Weizmann Institute of Science (Israel)Utrecht University (Netherlands)Universidad de Ciencias y Artes ... (Mexico)
Mahidol University (Thailand)MTT Agrifood Research Finland (Finland)University of British Columbia (Canada)Washington State University (USA)
University of Madras (India)Amity University (India)University of Melbourne (Australia)
||Sodium danshensu (SDSS), the sodium salt of danshensu (DSS), has the neuroprotective effect against cerebral I/R injury, and the potential mechanism might to inhibition of apoptosis through activating the PI3K/Akt signal pathway. SDSS has a protective effect against the genotoxicity of cigarette smoke，it shows a biphasic effects on vessel tension, while low dosage of sodium danshensu produces small contraction possibly through transient enhancement of Ca(2+) influx, high dosage produces significant vasodilation mainly through promoting the opening of non-selective K(+) channels and small-conductance calcium-sensitive K(+) channels in the vascular smooth muscle cells. |
||Calcium Channel | Potassium Channel | Akt | GSK-3 | Bcl-2/Bax | PI3K|
|Drugs & Clinic, 2014, 29(1):21-6. |
|Protection of flavonoid components baicalein,quercetin,or sodium danshensu on cytotoxicity and cellular DNA damage induced by cigarette smoke[Reference: WebLink]|
| To evaluate the protective effect of flavonoid components baicalein, quercetin or Sodium Danshensu on cytotoxicity and cellular DNA damage induced by cigarette smoke. Methods Two kinds of eukaryotic cells B-16 cells and oral buccal mucosal cells in liquid were attacked by the mainstream smoke produced via on-line cigarette smoking according to FTC with or without baicalein, quercetin or Sodium Danshensu. The cytotoxicity and cellular DNA damage were respectively assessed by MTT method and single cell gel electrophoresis. Results The cytotoxicity of B-16 cells and DNA damage of two kinds of cells induced by on-line cigarette smoking were obvious. A positive relationship was observed between the exposure time in smoke and the tail moment and olive tail moment of comet cells. Baicalein, quercetin, or Sodium Danshensu(1 mmol/L) could relieve the cytotoxicity by about 50% and decrease the DNA damage by more than 60%. Conclusion There is a positive relationship between the exposure of cells in smoke and the cellular DNA damage, and the flavonoid components baicalein, quercetin, or Sodium Danshensu have a protective effect against the genotoxicity of cigarette smoke.|
|Acta Pharmacol Sin. 2010 Apr;31(4):421-8. |
|Biphasic effects of sodium danshensu on vessel function in isolated rat aorta.[Pubmed: 20228827]|
|To investigate the effects of Sodium Danshensu on vessel function in isolated rat aortic ring.
METHODS AND RESULTS:
Thoracic aortae from normal rats were isolated and equilibrated in organ bath with Krebs-Henseleit buffer and ring tension was recorded. Effects of Sodium Danshensu on basal tonus of the vessel and its effects on vessel contraction and relaxation with or without endothelium were observed.
In thoracic arteries under basal tonus, Sodium Danshensu (0.3-3 g/L) produced a dose-dependent transient contraction. In phenylephrine-precontracted thoracic arteries with or without endothelium, low concentration (0.1-0.3 g/L) of Sodium Danshensu produced a weak contraction, while high concentrations (1-3 g/L) produced a pronounced vasodilator after a transient vasocontraction. Pre-incubation with Sodium Danshensu could inhibit vessel contraction induced by phenylephrine and potassium chloride in a concentration-dependent way. Sodium Danshensu inhibited phenylephrine- and CaCl(2)-induced vasoconstriction in Ca(2+)-free medium. Pre-incubation with tetraethylammonium, a non-selective K(+) channel blocker, and apamin, a small-conductance calcium-activated K(+) channel blocker partially antagonized the relaxation response induced by Sodium Danshensu. However, iberiotoxin (big-conductance calcium-sensitive K(+) channel blocker), barium chloride (inward rectifier K(+) channel blocker), and glibencalmide (ATP-sensitive K(+) channel blocker) had no influence on the vasodilation effect of Sodium Danshensu.
Sodium Danshensu showed a biphasic effects on vessel tension. While low dosage of Sodium Danshensu produced small contraction possibly through transient enhancement of Ca(2+) influx, high dosage produced significant vasodilation mainly through promoting the opening of non-selective K(+) channels and small-conductance calcium-sensitive K(+) channels in the vascular smooth muscle cells.
Sodium Danshensu Description
||The roots of Salvia miltiorrhiza Bge.
||DMSO, Pyridine, Methanol, Ethanol, 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.
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.2017.12.030.PMID: 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. 2015 Feb 15;22(2):283-9. |
|Neuroprotective effect and underlying mechanism of sodium danshensu [3-(3,4-dihydroxyphenyl) lactic acid from Radix and Rhizoma Salviae miltiorrhizae = Danshen] against cerebral ischemia and reperfusion injury in rats.[Pubmed: 25765834 ]|
|Sodium Danshensu (SDSS), the sodium salt of danshensu (DSS), has the same pharmacological effects as DSS.
METHODS AND RESULTS:
In the present study, we aimed to investigate the neuroprotective effect and possible mechanism of SDSS against cerebral ischemic/reperfusion injury. Sprague-Dawley rats were randomly divided into four groups: sham, control, 30 mg/kg and 60 mg/kg SDSS. Cerebral ischemia was induced by 2 h of middle cerebral artery occlusion (MCAO). Neurological functional deficits were evaluated according to the modified neurological severity score (mNSS); cerebral infarct volume and histological damage were measured by TTC or H-E staining. In addition, the number of apoptotic cells and caspase 3/7 activity were assessed by TUNEL or Caspase-Glo assay. And the expression of apoptosis-regulatory proteins and the PI3K/Akt pathway were investigated by western blotting. Our results showed that treatment with SDSS for 5 days after MCAO remarkably improved neurologic deficits and survival rate, reduced infarct volume and the number of dead neurons. SDSS also decreased the number of apoptotic cells, regulated the expression of Bcl-2 and Bax, and increased the ratio of Bcl-2/Bax. Further study revealed that treatment with SDSS also increased the level of p-Akt and p-GSK-3β.
Taken together, our results suggest that SDSS has the neuroprotective effect against cerebral I/R injury, and the potential mechanism might to inhibition of apoptosis through activating the PI3K/Akt signal pathway.