|Source:||The herb of Astragalus membranaceus Bge. var. mongholicus.|
|Biological Activity or Inhibitors:||1. Calycosin-7-O-β-d-glucoside can protect BBB integrity in experimental cerebral ischemia–reperfusion injury via regulating NO/cav-1/MMPs pathway.
2. Calycosin-7-O-β-D-glucoside can promote oxidative stress-induced cytoskeleton reorganization through integrin-linked kinase signaling pathway in vascular endothelial cells.
3. Calycosin-7-O-β-d-glucoside attenuates ischemia-reperfusion injuryin vivovia activation of the PI3K/Akt pathway.
4. Calycosin-7-O-β-D-glucoside has effects on cell apoptosis in cervical cancer HeLa cells and expression of Bcl-2/Bax.
|Solvent:||DMSO, Pyridine, Methanol, Ethanol, 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||2.2401 mL||11.2007 mL||22.4014 mL||44.8029 mL||56.0036 mL|
|5 mM||0.448 mL||2.2401 mL||4.4803 mL||8.9606 mL||11.2007 mL|
|10 mM||0.224 mL||1.1201 mL||2.2401 mL||4.4803 mL||5.6004 mL|
|50 mM||0.0448 mL||0.224 mL||0.448 mL||0.8961 mL||1.1201 mL|
|100 mM||0.0224 mL||0.112 mL||0.224 mL||0.448 mL||0.56 mL|
J Ethnopharmacol. 2014 Aug 8;155(1):692-701.
|Calycosin-7-O-β-D-glucoside regulates nitric oxide /caveolin-1/matrix metalloproteinases pathway and protects blood-brain barrier integrity in experimental cerebral ischemia-reperfusion injury.[Pubmed: 24930357]|
|Calycosin-7-O-beta-D-glucoside treatment significantly reduced infarct volume, histological damage and BBB permeability in the in vivo MCAO ischemia-reperfusion rat model. Calycosin-7-O-beta-D-glucoside treatment remarkably inhibited the expression and activities of MMPs, and secured the expression of cav-1 and tight junction proteins in the microvessels isolated from ischemic rat cortex. Furthermore, Calycosin-7-O-beta-D-glucoside was revealed to scavenge NO, inhibit the activities of MMP-2 and MMP-9, and attenuate cell death in the in vitro cultured brain microvascular endothelial cells under OGD condition.|
J Chromatogr B Analyt Technol Biomed Life Sci. 2014 Jul 15;963:16-23.
|Analysis of interaction property of calycosin-7-O-β-D-glucoside with human gut microbiota.[Pubmed: 24922599]|
|The results indicated that hydrolysis, demethylation, dehydroxylation and acetylation were the major metabolism of Calycosin-7-O-beta-D-glucoside. On the other hand, different strains of intestinal bacteria have varying degrees of growth sensitivity to Calycosin-7-O-beta-D-glucoside. Growth of certain pathogenic bacteria such as Enterobacter, Enterococcus, Clostridium and Bacteroides was significantly repressed by Calycosin-7-O-beta-D-glucoside, while commensal probiotics such as Lactobacillus, Bifidobacterium were less severely affected. This indicates that Calycosin-7-O-beta-D-glucoside exert significant effects on the intestinal environment by modulation of the intestinal bacterial population. Our observation provided further evidence for the importance of intestinal bacteria in the metabolism, absorption and potential activity of Calycosin-7-O-beta-D-glucoside in human health and diseases.|
Bmc Compl. Altern. M., 2015, 15(1):1-11.
|Calycosin-7-O-β-D-glucoside promotes oxidative stress-induced cytoskeleton reorganization through integrin-linked kinase signaling pathway in vascular endothelial cells.[Pubmed: 26346982 ]|
|Calycosin-7-O-beta-D-glucoside improved cell viability, suppressed apoptosis and protected the cells from LPS-induced reduction in cell migration and generation of ROS, protein level of NOS at a comparable magnitude to that of Y27632 and valsartan. Similar to Y27632 and valsartan, Calycosin-7-O-beta-D-glucoside, also neutralized LPS-induced actomyosin contraction and vinculin protein aggregation. Microarray assay, real-time PCR and western blot results revealed that LPS induced expression of FN, ITG A5, RhoA, PI3K (or PIP2 in western blotting), FAK, VEGF and VEGF R2, and inhibited expression of MLCP. We believed multiple pathways involved in the regulation of calycosin on HUVECs. Calycosin-7-O-beta-D-glucoside are considered to be able to activate MLCP through promoting the generation of NO, decreasing PMLC, suppressing the cytoskeleton remodeling caused by activation of Rho/ROCK pathway and inhibiting AKT pathway by decreasing VEGF, VEGF R2 and PI3K level.Conclusion Calycosin-7-O-beta-D-glucoside protected HUVEC from LPS-induced endothelial injury, possibly through suppression of Rho/ROCK pathway and regulation of AKT pathway.|
Mol Med Rep. 2016 Jan; 13(1): 633–640.
|Calycosin-7-O-β-d-glucoside attenuates ischemia-reperfusion injury in vivo via activation of the PI3K/Akt pathway[Pubmed: 26648122]|
|The results demonstrated that pretreatment with high dose (H)-CG markedly improved cardiac function, as evidenced by upregulated EF, FS and LVESP, and downregulated LVEDP. In addition, administration of Calycosin-7-O-beta-D-glucoside resulted in significant decreases in infarct size in the I/R+low dose-Calycosin-7-O-beta-D-glucoside and I/R+H-Calycosin-7-O-beta-D-glucoside groups, compared with the I/R group. The activities of CK and LDH, and the levels of MDA in the I/R+H-Calycosin-7-O-beta-D-glucoside group were reduced, compared with those in the I/R group, whereas SOD activity was elevated. Treatment with Calycosin-7-O-beta-D-glucoside inhibited the cleavage and activity of caspase-3 and caspase-9, and enhanced the phosphorylation of PI3K p85 and Akt. Notably, administration of the PI3K inhibitor, LY294002, markedly lowered the levels of p-PI3K p85/p-Akt, and eradicated the inhibitory effects of H-Calycosin-7-O-beta-D-glucoside on infarct size, myocardial injury and oxidative stress-induced damage. Taken together, the results suggested that Calycosin-7-O-beta-D-glucoside may alleviate I/R injury by activating the PI3K/Akt signaling pathway.|
Chinese Traditional & Herbal Drugs, 2015, 46(10):1498-502.
|Effects of calycosin-7-O-β-D-glucoside on cell apoptosis in cervical cancer HeLa cells and expression of Bcl-2/Bax[Reference: WebLink]|
|To explore the effect of Calycosin-7-O-beta-D-glucoside (CG) on apoptosis in cervical cancer HeLa cells and expression of Bcl-2/Bax. Methods: HeLa cells were cultured and divided into two groups, including control group and experimental group. Cell viabilities were determined by the MTT method; Apoptosis and cell cycle were analyzed by flow cytometry; The changes of protein expression of cleaved Caspase-3, Bcl-2, and Bax were detected by Western blotting. Results: From the data of MTT, the cell proliferation of human cervical cancer HeLa cells was inhibited by CG (2.5-100 μg/mL) in a dose- and time-dependent manner. Flow cytometry assays showed that EGCG significantly induced the apoptosis in HeLa cells. The apoptosis rate of the experimental group were increased gradually in 48 h after treated with CG (20, 40, and 80 μg/mL), they were 10.40%, 25.50%, and 39.40%, respectively, significantly higher than those in the control group. The data of Western blotting showed that CG down-regulated Bcl-2 and up-regulated cleaved Caspase-3 and Bax in a dose-dependent manner. Conclusion: CG could inhibit the the proliferation of HeLa cells and promote apoptosis, and the anticancer effect of CG may be associated with the down-regulation of Bcl-2 expression and up-regulation of Bax expression, as well as the increase of relative activity of Caspase-3. CG may be a promising antitumor agent for cancer treatment.|