Diammonium glycyrrhizinateCAS# 79165-06-3 |
Quality Control & MSDS
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| Cas No. | 79165-06-3 | SDF | Download SDF |
| PubChem ID | 656656 | Appearance | Powder |
| Formula | C42H68N2O16 | M.Wt | 857.00 |
| Type of Compound | Triterpenoids | Storage | Desiccate at -20°C |
| Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
| Chemical Name | (2S,3S,4S,5R,6R)-6-[(2S,3R,4S,5S,6S)-2-[[(3S,4aR,6aR,6bS,8aS,11S,12aR,14aR,14bS)-11-carboxy-4,4,6a,6b,8a,11,14b-heptamethyl-14-oxo-2,3,4a,5,6,7,8,9,10,12,12a,14a-dodecahydro-1H-picen-3-yl]oxy]-6-carboxy-4,5-dihydroxyoxan-3-yl]oxy-3,4,5-trihydroxyoxane-2-carboxylic acid;azane | ||
| SMILES | CC1(C2CCC3(C(C2(CCC1OC4C(C(C(C(O4)C(=O)O)O)O)OC5C(C(C(C(O5)C(=O)O)O)O)O)C)C(=O)C=C6C3(CCC7(C6CC(CC7)(C)C(=O)O)C)C)C)C.N.N | ||
| Standard InChIKey | SPPIIOPGDLITJE-VLQRKCJKSA-N | ||
| Standard InChI | InChI=1S/C42H62O16.2H3N/c1-37(2)21-8-11-42(7)31(20(43)16-18-19-17-39(4,36(53)54)13-12-38(19,3)14-15-41(18,42)6)40(21,5)10-9-22(37)55-35-30(26(47)25(46)29(57-35)33(51)52)58-34-27(48)23(44)24(45)28(56-34)32(49)50;;/h16,19,21-31,34-35,44-48H,8-15,17H2,1-7H3,(H,49,50)(H,51,52)(H,53,54);2*1H3/t19-,21-,22-,23-,24-,25-,26-,27+,28-,29-,30+,31+,34-,35-,38+,39-,40-,41+,42+;;/m0../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. |
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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. Diammonium glycyrrhizinate shows antiviral effect on cell infection by pseudorabies herpesvirus. 2. Diammonium Glycyrrhizinate can reduce inflammatory injury in a rat model of ulcerative colitis, this may occur via suppression of NF-kappaB, TNF-alpha and ICAM-1 in colonic mucosa. 3. Diammonium glycyrrhizinate may possibly protect the liver from injury via two pathways: direct protection of hepatocytes from apoptosis through an IL-6-dependent way and indirect inhibition of T-cell-mediated inflammation through an IL-10-dependent way. 4. Diammonium glycyrrhizinate can attenuate Aβ(1-42)-induced neuronal injury by preventing mitochondrial dysfunction and oxidative stress and improve cognitive impairment in Aβ(1-42)-induced AD mice, indicating that it exerts potential beneficial effects on AD. 5. Diammonium glycyrrhizinate can inhibit airway smooth muscle proliferation possibly through up- regulation of PPARγ in a murine model of chronic asthma. |
| Targets | NF-kB | TNF-α | IL Receptor | ROS | Beta Amyloid | Caspase | PPAR | Antifection |
Diammonium glycyrrhizinate Dilution Calculator
Diammonium glycyrrhizinate Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 1.1669 mL | 5.8343 mL | 11.6686 mL | 23.3372 mL | 29.1715 mL |
| 5 mM | 0.2334 mL | 1.1669 mL | 2.3337 mL | 4.6674 mL | 5.8343 mL |
| 10 mM | 0.1167 mL | 0.5834 mL | 1.1669 mL | 2.3337 mL | 2.9172 mL |
| 50 mM | 0.0233 mL | 0.1167 mL | 0.2334 mL | 0.4667 mL | 0.5834 mL |
| 100 mM | 0.0117 mL | 0.0583 mL | 0.1167 mL | 0.2334 mL | 0.2917 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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[Diammonium glycyrrhizinate inhibits airway smooth muscle proliferation in a murine model of chronic asthma].[Pubmed:24144738]
Nan Fang Yi Ke Da Xue Xue Bao. 2013 Oct;33(10):1416-20.
OBJECTIVE: To investigate the therapeutic value and possible mechanism of Diammonium glycyrrhizinate (DG) in treatment of airway remodeling in a murine model of chronic asthma. METHODS: Thirty male BALB/C mice were randomly divided into control group, OVA+DG group and OVA group (n=10). HE staining was used to observe the pathological changes, and Masson's staining was used to detect and measure collagen deposition. Alpha-SMA and PPARgamma mRNA expressions were analyzed by RT-PCR, and the protein expressions of alpha-SMA and PPARgamma were measured by Western blotting. RESULTS: After 75 days of OVA sensitization and challenge, obvious pathological changes occurred in the lung tissues, which was more severe in OVA group than in OVA+DG group. Collagen deposition was significantly increased after OVA stimulation, but was obviously milder in OVA+DG group than in OVA group. OVA-induced up-regulation of alpha-SMA was notably attenuated by DG injection. The expression of PPARgamma was markedly down-regulated after OVA stimulation but was substantially enhanced after DG intervention. CONCLUSION: DG can inhibit airway smooth muscle proliferation possibly through up-regulation of PPARgamma in a murine model of chronic asthma.
Diammonium glycyrrhizinate, a component of traditional Chinese medicine Gan-Cao, prevents murine T-cell-mediated fulminant hepatitis in IL-10- and IL-6-dependent manners.[Pubmed:17673144]
Int Immunopharmacol. 2007 Oct;7(10):1292-8.
Diammonium glycyrrhizinate (DG), a traditional Chinese medicine (TCM), is extracted and purified from liquorices (Radix glycyrrhizae). The liquorices exert an important function in the treatment of hepatitis because of its anti-inflammatory effects based upon the clinical practice, but the underlying mechanism is unclear. In this study, we investigated the mechanisms of DG in protecting mice from ConA-induced hepatitis. The results showed that intraperitoneal administration of DG protected mice against ConA-induced elevation of serum ALT levels and apoptosis of hepatocytes; at the same time, the absolute amount of hepatic NKT cells and T cells was significantly decreased, indicating that DG can inhibit the recruitment of lymphocytes into the liver. In addition, the production of IL-6 and IL-10 was improved by DG pretreatment, suggesting that DG may possibly protect the liver from injury via two pathways: direct protection of hepatocytes from apoptosis through an IL-6-dependent way and indirect inhibition of T-cell-mediated inflammation through an IL-10-dependent way.
Anti-inflammatory effect of Diammonium Glycyrrhizinate in a rat model of ulcerative colitis.[Pubmed:16874877]
World J Gastroenterol. 2006 Jul 28;12(28):4578-81.
AIM: To explore the anti-inflammatory mechanism of Diammonium glycyrrhizinate in a rat model of ulcerative colitis induced by acetic acid. METHODS: Spragur-Dawley female rats were divided into four groups: Diammonium glycyrrhizinate group, dexamethasone group, acetic acid control and normal control group. Colonic inflammation was evaluated by disease activity index, gross morphologic damage, histological injury and colonic myeloperoxidase activity. Immunohistochemistry was used to detect the expression of NF-kappaB, TNF-alpha and ICAM-1 in colonic mucosa. RESULTS: Compared to the acetic acid control, both Diammonium glycyrrhizinate and dexamethasone showed a significant anti-inflammatory effect (P < 0.01). The expression of NF-kappaB, TNF-alpha and ICAM-1 in colonic mucosa was significantly lower in the Diammonium glycyrrhizinate group and dexamethasone group than in the acetic acid group. CONCLUSION: Diammonium glycyrrhizinate could reduce inflammatory injury in a rat model of ulcerative colitis. This may occur via suppression of NF-kappaB, TNF-alpha and ICAM-1 in colonic mucosa.
Antiviral effect of diammonium glycyrrhizinate and lithium chloride on cell infection by pseudorabies herpesvirus.[Pubmed:19879899]
Antiviral Res. 2010 Feb;85(2):346-53.
Diammonium glycyrrhizin (DG), a salt from glycyrrhizinate (GL) that is a major active component of licorice root extract with various pharmacological activities was investigated for its inhibitory effect on pseudorabies virus (PrV) infection. In parallel, lithium chloride (LiCl), a chemical reagent with potential antiviral activity was compared with DG for their inhibitory ability against PrV infection in vitro. Virus plaque-reduction assays, PCR and RT-PCR analysis indicated that both drugs inhibited cell infection by PrV. Moreover, addition of the drugs resulted in fewer apoptotic cells during PrV infection.
Diammonium glycyrrhizinate upregulates PGC-1alpha and protects against Abeta1-42-induced neurotoxicity.[Pubmed:22540007]
PLoS One. 2012;7(4):e35823.
Mitochondrial dysfunction is a hallmark of beta-amyloid (Abeta)-induced neurotoxicity in Alzheimer's disease (AD), and is considered an early event in AD pathology. Diammonium glycyrrhizinate (DG), the salt form of Glycyrrhizin, is known for its anti-inflammatory effects, resistance to biologic oxidation and membranous protection. In the present study, the neuroprotective effects of DG on Abeta(1-42)-induced toxicity and its potential mechanisms in primary cortical neurons were investigated. Exposure of neurons to 2 microM Abeta(1-42) resulted in significant viability loss and cell apoptosis. Accumulation of reactive oxygen species (ROS), decreased mitochondrial membrane potential, and activation of caspase-9 and caspase-3 were also observed after Abeta(1-42) exposure. All these effects induced by Abeta(1-42) were markedly reversed by DG treatment. In addition, DG could alleviate lipid peroxidation and partially restore the mitochondrial function in Abeta(1-42)-induced AD mice. DG also significantly increased the PGC-1alpha expression in vivo and in vitro, while knocking down PGC-1alpha partially blocked the protective effects, which indicated that PGC-1alpha contributed to the neuroprotective effects of DG. Furthermore, DG significantly decreased the escape latency and search distance and increased the target crossing times of Abeta(1-42)-induced AD mice in the Morris water maze test. Therefore, these results demonstrated that DG could attenuate Abeta(1-42)-induced neuronal injury by preventing mitochondrial dysfunction and oxidative stress and improved cognitive impairment in Abeta(1-42)-induced AD mice, indicating that DG exerted potential beneficial effects on AD.
