AstringinCAS# 29884-49-9 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 29884-49-9 | SDF | Download SDF |
PubChem ID | 5281712 | Appearance | Powder |
Formula | C20H22O9 | M.Wt | 406.4 |
Type of Compound | Phenols | Storage | Desiccate at -20°C |
Synonyms | 3,3',4,5'-Tetrahydroxystilbene 3'-glucoside | ||
Solubility | DMSO : 150 mg/mL (369.11 mM; Need ultrasonic) | ||
Chemical Name | (2S,3R,4S,5S,6R)-2-[3-[(E)-2-(3,4-dihydroxyphenyl)ethenyl]-5-hydroxyphenoxy]-6-(hydroxymethyl)oxane-3,4,5-triol | ||
SMILES | C1=CC(=C(C=C1C=CC2=CC(=CC(=C2)OC3C(C(C(C(O3)CO)O)O)O)O)O)O | ||
Standard InChIKey | PERPNFLGJXUDDW-CUYWLFDKSA-N | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
Description | 1. Astringinin is a potent antiarrhythmic agent with cardioprotective activity in ischemic and ischemic-reperfused rat heart, the beneficial effects of astringinin in the ischemic and ischemic-reperfused hearts may be correlated with its antioxidant activity and upregulation of NO production. 2. Astringinin can significantly attenuate proinflammatory responses and hepatic injury after trauma-hemorrhage, the salutary effects of astringinin administration on attenuation of hepatic injury following trauma-hemorrhage are likely due to reduction of pro-inflammatory mediator levels. |
Targets | NO | IL Receptor |
Astringin Dilution Calculator
Astringin Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.4606 mL | 12.3031 mL | 24.6063 mL | 49.2126 mL | 61.5157 mL |
5 mM | 0.4921 mL | 2.4606 mL | 4.9213 mL | 9.8425 mL | 12.3031 mL |
10 mM | 0.2461 mL | 1.2303 mL | 2.4606 mL | 4.9213 mL | 6.1516 mL |
50 mM | 0.0492 mL | 0.2461 mL | 0.4921 mL | 0.9843 mL | 1.2303 mL |
100 mM | 0.0246 mL | 0.123 mL | 0.2461 mL | 0.4921 mL | 0.6152 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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Beneficial effects of astringinin, a resveratrol analogue, on the ischemia and reperfusion damage in rat heart.[Pubmed:11295530]
Free Radic Biol Med. 2001 Apr 15;30(8):877-83.
Oxidative stress plays an important role in the pathogenesis of myocardial ischemia and infarction. Antioxidants might then be beneficial in the prevention of these diseases. Astringinin (3,3',4',5-tetrahydroxystilbene), a resveratrol (3,4',5-trihydroxystilbene) analogue with considerably higher antioxidative activity and free radical scavenging capacity, was introduced to examine its cardioprotective effects in ischemia or ischemia-reperfusion (I/R) rats. In the present study, the left main coronary artery was occluded by the following procedures: (i) 30 min occlusion, (ii) 5 min occlusion followed by 30 min reperfusion, and (iii) 4 h occlusion. Animals were infused with and without Astringinin before coronary artery occlusion. Mortality, and the severity of ischemia- and I/R-induced arrhythmias were compared. Pretreatment of Astringinin dramatically reduced the incidence and duration of ventricular tachycardia (VT) and ventricular fibrillation (VF) during either ischemia or I/R period. Astringinin at 2.5 x 10(-5) and 2.5 x 10(-4) g/kg completely prevented the mortality of animals during ischemia or I/R. During the same period, Astringinin pretreatment also increased nitric oxide (NO) and decreased lactate dehydrogenase (LDH) levels in the carotid blood. In animals subjected to 4 h coronary occlusion, the cardiac infarct size (expressed as a percentage of occluded zone) was reduced from 44.4 + or - 4.1% to 19.1 + or - 2.4% by Astringinin (2.5 x 10(-4) g/kg). We conclude that, Astringinin is a potent antiarrhythmic agent with cardioprotective activity in ischemic and ischemic-reperfused rat heart. The beneficial effects of Astringinin in the ischemic and ischemic-reperfused hearts may be correlated with its antioxidant activity and upregulation of NO production.
Astringinin-mediated attenuation of the hepatic injury following trauma-hemorrhage.[Pubmed:21789900]
Chin J Physiol. 2011 Jun 30;54(3):183-9.
Although Astringinin administration under adverse circulatory conditions is known to be protective, the mechanism by which Astringinin produces the salutary effects remains unknown. We hypothesize that Astringinin administration in males following trauma-hemorrhage decreases cytokine production and protects against hepatic injury. Male Sprague-Dawley rats underwent trauma-hemorrhage (mean blood pressure: 40 mmHg for 90 min, then resuscitation). Different doses of Astringinin (0.01, 0.03, 0.1, 0.3 mg/kg of body weight) or vehicle were administered intravenously during resuscitation. Concentrations of plasma aspartate aminotransferase (AST) with alanine aminotransferase (ALT) and various hepatic parameters were measured (n = 8 rats/group) at 24 h after resuscitation. One-way ANOVA and Tukey testing were used for statistical analysis. Trauma-hemorrhage significantly increased plasma AST and ALT levels at 24 h postresuscitation; there was a dose-related benefit when Astringinin was administered at doses of 0.01 to 0.3 mg/kg. In Astringinin-treated (0.3 mg/kg) rats subjected to trauma-hemorrhage, there were significant improvements in liver myeloperoxidase (MPO) activity (237.80 +/- 45.89 vs. 495.95 +/- 70.64 U/mg protein, P < 0.05), interleukin-6 (IL-6) levels (218.54 +/- 34.52 vs. 478.60 +/- 76.21 pg/mg protein, P < 0.05), cytokine-induced neutrophil chemoattractant (CINC)-1 (88.32 +/- 20.33 vs. 200.70 +/- 32.68 pg/mg protein, P < 0.05), CINC-3 (110.83 +/- 26.63 vs. 290.14 +/- 76.82 pg/mg protein, P < 0.05) and intercellular adhesion molecule (ICAM)-1 concentrations (1,868.5 +/- 211.5 vs. 3,645.0 +/- 709.2 pg/mg protein, P < 0.05), as well as in histology. Results show that Astringinin significantly attenuates proinflammatory responses and hepatic injury after trauma-hemorrhage. In conclusion, the salutary effects of Astringinin administration on attenuation of hepatic injury following trauma-hemorrhage are likely due to reduction of pro-inflammatory mediator levels.