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Vitexin argininate

CAS# 51542-56-4

Vitexin argininate

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Chemical structure

Vitexin argininate

3D structure

Chemical Properties of Vitexin argininate

Cas No. 51542-56-4 SDF Download SDF
PubChem ID 102004660 Appearance Yellow powder
Formula C27H34N4O12 M.Wt 606.6
Type of Compound Flavonoids Storage Desiccate at -20°C
Solubility Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
Chemical Name (2S)-2-amino-5-(diaminomethylideneamino)pentanoic acid;5,7-dihydroxy-2-(4-hydroxyphenyl)-8-[(2S,3R,4R,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]chromen-4-one
SMILES CC1C(C(C(C(O1)OC2C(C(C(OC2OC3CC4(C(CC(C5C4(CCC5C(C)(CCC=C(C)C)OC6C(C(C(C(O6)CO)O)O)O)C)O)C7(C3C(C(CC7)O)(C)C)C)C)CO)O)O)O)O)O
Standard InChIKey UYXWSGOMVDZQBF-ZKSSNEHASA-N
Standard InChI InChI=1S/C21H20O10.C6H14N4O2/c22-7-14-17(27)18(28)19(29)21(31-14)16-11(25)5-10(24)15-12(26)6-13(30-20(15)16)8-1-3-9(23)4-2-8;7-4(5(11)12)2-1-3-10-6(8)9/h1-6,14,17-19,21-25,27-29H,7H2;4H,1-3,7H2,(H,11,12)(H4,8,9,10)/t14-,17-,18+,19-,21+;4-/m10/s1
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.
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.
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.

Source of Vitexin argininate

The seeds of Vitex trifolia L.

Vitexin argininate Dilution Calculator

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Vitexin argininate Molarity Calculator

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Preparing Stock Solutions of Vitexin argininate

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.6485 mL 8.2427 mL 16.4853 mL 32.9707 mL 41.2133 mL
5 mM 0.3297 mL 1.6485 mL 3.2971 mL 6.5941 mL 8.2427 mL
10 mM 0.1649 mL 0.8243 mL 1.6485 mL 3.2971 mL 4.1213 mL
50 mM 0.033 mL 0.1649 mL 0.3297 mL 0.6594 mL 0.8243 mL
100 mM 0.0165 mL 0.0824 mL 0.1649 mL 0.3297 mL 0.4121 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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References on Vitexin argininate

Ginsenoside Re protects methamphetamine-induced dopaminergic neurotoxicity in mice via upregulation of dynorphin-mediated kappa-opioid receptor and downregulation of substance P-mediated neurokinin 1 receptor.[Pubmed:29467000]

J Neuroinflammation. 2018 Feb 21;15(1):52.

BACKGROUND: We previously reported that ginsenoside Re (GRe) attenuated against methamphetamine (MA)-induced neurotoxicity via anti-inflammatory and antioxidant potentials. We also demonstrated that dynorphin possesses anti-inflammatory and antioxidant potentials against dopaminergic loss, and that balance between dynorphin and substance P is important for dopaminergic neuroprotection. Thus, we examined whether GRe positively affects interactive modulation between dynorphin and substance P against MA neurotoxicity in mice. METHODS: We examined changes in dynorphin peptide level, prodynorphin mRNA, and substance P mRNA, substance P-immunoreactivity, homeostasis in enzymatic antioxidant system, oxidative parameter, microglial activation, and pro-apoptotic parameter after a neurotoxic dose of MA to clarify the effects of GRe, prodynorphin knockout, pharmacological inhibition of kappa-opioid receptor (i.e., nor-binaltorphimine), or neurokinin 1 (NK1) receptor (i.e., L-733,060) against MA insult in mice. RESULTS: GRe attenuated MA-induced decreases in dynorphin level, prodynorphin mRNA expression in the striatum of wild-type (WT) mice. Prodynorphin knockout potentiated MA-induced dopaminergic toxicity in mice. The imbalance of enzymatic antioxidant system, oxidative burdens, microgliosis, and pro-apoptotic changes led to the dopaminergic neurotoxicity. Neuroprotective effects of GRe were more pronounced in prodynorphin knockout than in WT mice. Nor-binaltorphimine, a kappa-opioid receptor antagonist, counteracted against protective effects of GRe. In addition, we found that GRe significantly attenuated MA-induced increases in substance P-immunoreactivity and substance P mRNA expression in the substantia nigra. These increases were more evident in prodynorphin knockout than in WT mice. Although, we observed that substance P-immunoreactivity was co-localized in NeuN-immunreactive neurons, GFAP-immunoreactive astrocytes, and Iba-1-immunoreactive microglia. NK1 receptor antagonist L-733,060 or GRe selectively inhibited microgliosis induced by MA. Furthermore, L-733,060 did not show any additive effects against GRe-mediated protective activity (i.e., antioxidant, antimicroglial, and antiapoptotic effects), indicating that NK1 receptor is one of the molecular targets of GRe. CONCLUSIONS: Our results suggest that GRe protects MA-induced dopaminergic neurotoxicity via upregulatgion of dynorphin-mediated kappa-opioid receptor and downregulation of substance P-mediated NK1 R.

Salvianolic Acid B and Ginsenoside Re Synergistically Protect Against Ox-LDL-Induced Endothelial Apoptosis Through the Antioxidative and Antiinflammatory Mechanisms.[Pubmed:29973885]

Front Pharmacol. 2018 Jun 20;9:662.

Salvianolic acid B (SalB) and ginsenoside Re (Re) protect endotheliocytes against apoptosis through different mechanisms. However, whether both compounds could synergistically protect endothelial cells against oxidized low-density lipoprotein (Ox-LDL)-induced apoptosis is unclear. This study aimed to assess the protective effect of combined SalB and Re (SR) treatment on Ox-LDL-induced endothelial apoptosis and to explore the mechanism underlying this effect. Results showed that SalB, Re, or SR could protect against Ox-LDL-induced endothelial apoptosis. Furthermore, the composition of SR was optimized through central composite design with response surface methodology. SR with a composition of 60 mug/mL of SalB and 120 mug/mL of Re exerted the optimal protective effect. Network pharmacology research revealed that SalB and Re in SR synergistically protect against Ox-LDL-induced endothelial apoptosis by regulating oxidative stress and phlogistic pathways. In vitro experiments confirmed these results. Compared with the same dose of SalB or Re alone, SR significantly decreased the contents of inflammatory mediators and increased the activities of antioxidant enzymes. SR could synergistically restore the balanced redox state of the cells and inhibit the activation of nuclear transcription factor kappa B and the caspase cascade by activating the phosphatidylinositol 3 kinase/protein kinase B pathway and inhibiting the phosphorylation of p38 mitogen-activated protein kinase. These pathways are regulated by down-regulating the expression of lectin-like Ox-LDL receptor-1 and NADPH oxidase and up-regulating the expression of estrogen receptor alpha. Therefore, SR effectively prevents Ox-LDL-induced endothelial apoptosis through antioxidative and antiinflammatory mechanisms.

Changes in intestinal microbiota affect metabolism of ginsenoside Re.[Pubmed:29748959]

Biomed Chromatogr. 2018 Oct;32(10):e4284.

Ginsenoside Re, an active ingredient in Panax ginseng, is widely used as a therapeutic and nutriment. The intestinal microbiota plays crucial roles in modulating the pharmacokinetics and pharmacological actions of ginsenoside Re. The aim of this study was to explore the relationship between bacterial community variety and the metabolic profiles of ginsenoside Re. We developed two models with intestinal dysbacteriosis: a pseudo-germ-free model induced by a nonabsorbable antimicrobial mixture (ATM), and Qi-deficiency model established via over-fatigue and acute cold stress (OACS). First, the bacterial community structures in control, ATM and OACS rats were compared via 16S ribosomal RNA amplicon sequencing. Then, the gut microbial metabolism of ginsenoside Re was assessed qualitatively and quantitatively in the three groups by UPLC-Q-TOF/MS and HPLC-TQ-MS, respectively. Ten metabolites of ginsenoside Re were detected and tentatively identified, three of which were novel. Moreover, owing to significant differences in bacterial communities, deglycosylated products, as the main metabolites of ginsenoside Re, were produced at lower levels in ATM and OACS models. Importantly, the levels of these deglycosylated metabolites correlated with alterations in Prevotella, Lactobacillus and Bacteroides populations, as well as glycosidase activities. Collectively, biotransformation of ginsenoside Re is potentially influenced by regulation of the composition of intestinal microbiota and glycosidase activities.

Defensive Properties of Ginsenoside Re against UV-B-Induced Oxidative Stress through Up-Regulating Glutathione and Superoxide Dismutase in HaCaT Keratinocytes.[Pubmed:29755556]

Iran J Pharm Res. 2018 Winter;17(1):249-260.

Ginseng is now used worldwide as a traditional Oriental medicine. Ginsenosides, also known as ginseng saponins, are responsible for most pharmacological efficacies of ginseng. This work aimed to assess the novel skin anti-photoaging potential of ginsenoside Re (Re), a protopanaxatriol-type ginsenoside, by analyzing reactive oxygen species (ROS), pro-matrix metalloproteinase-2 (proMMP-2) and -9 (proMMP-9), total glutathione (GSH), superoxide dismutase (SOD), and cellular viability in UV-B-irradiated HaCaT keratinocytes. When HaCaT cells were pretreated with Re prior to UV-B irradiation, Re significantly suppressed the UV-B-induced ROS elevation. It was also able to attenuate the UV-B-induced proMMP-2 and -9 elevations at both activity and protein levels. Re was capable of overcoming the UV-B-reduced total GSH content and SOD activity in concentration-dependent ways. Under the experimental conditions used, Re could interfere with cellular viabilities in neither non-irradiated nor UV-B-irradiated keratinocytes.

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