Astragaloside Aanti-hypertension, positive inotropic action, anti-inflammation, and anti-myocardial injury CAS# 83207-58-3 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 83207-58-3 | SDF | Download SDF |
PubChem ID | 122690 | Appearance | Powder |
Formula | C41H68O14 | M.Wt | 784.97 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Synonyms | Astramembrannin I; Astragalin A | ||
Solubility | DMSO : ≥ 50 mg/mL (63.70 mM) H2O : < 0.1 mg/mL (insoluble) *"≥" means soluble, but saturation unknown. | ||
SMILES | CC1(C(CCC23C1C(CC4C2(C3)CCC5(C4(CC(C5C6(CCC(O6)C(C)(C)O)C)O)C)C)OC7C(C(C(C(O7)CO)O)O)O)OC8C(C(C(CO8)O)O)O)C | ||
Standard InChIKey | QMNWISYXSJWHRY-XZFBGSIGSA-N | ||
Standard InChI | InChI=1S/C41H68O14/c1-35(2)24(54-33-29(48)26(45)20(44)17-51-33)9-11-41-18-40(41)13-12-37(5)31(39(7)10-8-25(55-39)36(3,4)50)19(43)15-38(37,6)23(40)14-21(32(35)41)52-34-30(49)28(47)27(46)22(16-42)53-34/h19-34,42-50H,8-18H2,1-7H3/t19-,20+,21-,22+,23-,24-,25-,26-,27?,28-,29+,30?,31-,32-,33-,34+,37+,38-,39+,40-,41+/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 | Astragaloside A is one of the major active constituents of Astragalus membranaceus in Traditional Chinese Medicine; has been widely used to treat ischemic diseases.
IC50 value:
Target:
in vitro: AS-IV treatment promotes umbilical vein endothelial cells (HUVEC) proliferation, migration, and tube formation. AS-IV treatment also activates JAK2/STAT3 and ERK1/2 signaling pathways, and up-regulates endothelial nitric oxide synthase (eNOS) expression and nitric oxide (NO) production [1]. Administration of astragaloside IV (16, 32, and 64 μM) 1 h prior to lipopolysaccharide stimulation dose-dependently attenuated cardiac hypertrophy induced by lipopolysaccharide. Further studies demonstrated that astragaloside IV inhibited the increment of the resting intracellular free Ca2+, and its effect was similar to verapamil [2]. ASI could inhibit cells apoptosis induced by high glucose (25mmol/L) in dose-dependent and time-dependent manners. ASI also inhibited high glucose-induced expression of TGF-β1 and activation of p38 MAPK pathway at the protein level. Furthermore, ASI increased HGF production in human tubular epithelial cells [3].
in vivo: the growth of tumor was suppressed by AS-IV treatment in vivo. AS-IV also could down-regulate regulatory T cells (Tregs) and up-regulate cytotoxic T lymphocytes (CTLs) in vivo and in vitro[4]. As an in vivo model, mice subjected to unilateral ureteral obstruction (UUO) were administered AS-IV (20 mg/kg) by intraperitoneal injection for 7 days. AS-IV significantly alleviated renal mass loss and reduced the expression of α-smooth muscle actin, fibronectin, and collagen IV both in vitro and in vivo [5]. References: |
Astragaloside A Dilution Calculator
Astragaloside A Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 1.2739 mL | 6.3697 mL | 12.7393 mL | 25.4787 mL | 31.8484 mL |
5 mM | 0.2548 mL | 1.2739 mL | 2.5479 mL | 5.0957 mL | 6.3697 mL |
10 mM | 0.1274 mL | 0.637 mL | 1.2739 mL | 2.5479 mL | 3.1848 mL |
50 mM | 0.0255 mL | 0.1274 mL | 0.2548 mL | 0.5096 mL | 0.637 mL |
100 mM | 0.0127 mL | 0.0637 mL | 0.1274 mL | 0.2548 mL | 0.3185 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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IC50: N/A
Astragaloside A (Astragaloside IV), a pure saponin isolated from Astragalus membranaceus Bge, exhibits several pharmacological actions, such as anti-hypertension, positive inotropic action, anti-inflammation, and anti-myocardial injury [1, 2]. Astragaloside IV has been widely used for the treatment of cardiovascular disorders and kidney disease [3].
In vitro: Astragaloside IV (2-40 μM) dose-dependently decreased TGF-β-induced a-SMA, fibronectin, CTGF, collagen I and III expression, up-regulated Smad7, but decreased p-Smad2 and p-Smad3 expression in NRK-49F cells [2]. Moreover, Astragaloside IV prevented tubular epithelial apoptosis partially through inhibiting MAPK pathway activity, thereby ameliorating renal fibrosis [3].
In vivo: Astragaloside IV (5 and 10 mg/kg/day, intraperitoneal injection) reduced serum lactate dehydrogenase and creatine kinase enzyme levels and attenuated this reduction in the Ca2+-ATPase activity in rats [1]. Astragaloside IV (3.33, 10, and 33 mg/kg, intraperitoneal injection) treatment attenuated renal damage and improved renal function through inhibiting TGF-β/Smad signaling pathway in a dose-dependent manner in unilateral ureteral obstruction kidneys [2].
References:
1. Xu XL, Ji H, Gu SY, Shao Q, Huang QJ, Cheng YP. Modification of alterations in cardiac function and sarcoplasmic reticulum by astragaloside IV in myocardial injury in vivo. Eur J Pharmacol. 2007;568(1-3):203-12.
2. Wang L, Chi YF, Yuan ZT, Zhou WC, Yin PH, Zhang XM, et al. Astragaloside IV inhibits renal tubulointerstitial fibrosis by blocking TGF-beta/Smad signaling pathway in vivo and in vitro. Exp Biol Med (Maywood). 2014;239(10):1310-24.
3. Xu W, Shao X, Tian L, Gu L, Zhang M, Wang Q, et al. Astragaloside IV ameliorates renal fibrosis via the inhibition of mitogen-activated protein kinases and antiapoptosis in vivo and in vitro. J Pharmacol Exp Ther. 2014;350(3):552-62.
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Astragaloside IV inhibits PMA-induced EPCR shedding through MAPKs and PKC pathway.[Pubmed:28367652]
Immunopharmacol Immunotoxicol. 2017 Jun;39(3):148-156.
Astragaloside IV (AS-IV), a main active substance isolated from Astragalus membranaceus Bunge, has been shown to have multiple pharmacological effects. Endothelial cell protein C receptor (EPCR) is a marker of inflammation, and is also a major member of protein C (PC) anti-coagulation system. EPCR can be cut off from the cell surface by tumor necrosis factor-alpha converting enzyme (TACE), which is controlled through mitogen-activated protein kinase (MAPK) and protein kinase C (PKC) pathways. To develop novel therapeutic drug for EPCR shedding, the effect of AS-IV was studied in phorbol-12-myristate 13-acetate (PMA)-induced human umbilical vein endothelial cells (HUVECs) and the potential molecular mechanism of AS-IV action was investigated. The results showed that AS-IV could significantly inhibit PMA-induced EPCR shedding. In further study, AS-IV suppressed the expression and activity of TACE. In addition, AS-IV could decrease the phosphorylation of MAPK such as janus kinase (JNK) and p38, and inhibit activation of PKC through the prevention of non-phosphorylation and phosphorylation of specific PKC isoforms in PMA-stimulated HUVECs. These findings indicate that AS-IV may be used as a natural medicine to treat EPCR-related systemic inflammation and cardiovascular diseases by targeting MAPK and PKC pathway.
Astragaloside IV attenuates free fatty acid-induced ER stress and lipid accumulation in hepatocytes via AMPK activation.[Pubmed:28344322]
Acta Pharmacol Sin. 2017 Jul;38(7):998-1008.
Although the pathogenesis of non-alcoholic fatty liver disease (NAFLD) is not completely understood, the increased influx of free fatty acids (FFAs) into the liver and the FFA-induced hepatic endoplasmic reticulum (ER) stress are two crucial pathogenic processes in the initiation and development of NAFLD. In this study we investigated the effects of astragaloside IV (AS-IV), a bioactive compound purified from Astragali Radix, on FFA-induced lipid accumulation in hepatocytes and elucidated the underlying mechanisms. Human HepG2 cells and primary murine hepatocytes were exposed to FFAs (1 mmol/L, oleate/palmitate, 2:1 ratio) with or without AS-IV for 24 h. Exposure to FFAs induced marked lipid accumulation in hepatocytes, whereas co-treatment with AS-IV (100 mug/mL) significantly attenuated this phenomenon. Notably, AS-IV (50-200 mug/mL) concentration-dependently enhanced the phosphorylation of AMPK, acetyl-CoA carboxylase (ACC) and SREBP-1c, inhibited the accumulation and nuclear translocation of mature SREBP-1 and subsequently decreased the mRNA levels of lipogenic genes including acc1, fas and scd1. AS-IV treatment also concentration-dependently attenuated FFA-induced hepatic ER stress evidenced by the reduction of the key markers, GRP78, CHOP and p-PERK. Pretreated the cells with the AMPK inhibitor compound C (20 mumol/L) greatly diminished these beneficial effects of AS-IV. Our results demonstrate that AS-IV attenuates FFA-induced ER stress and lipid accumulation in an AMPK-dependent manner in hepatocytes, which supports its use as promising therapeutics for hepatic steatosis.
Astragaloside IV Alleviates Lipopolysaccharide-Induced Acute Kidney Injury Through Down-Regulating Cytokines, CCR5 and p-ERK, and Elevating Anti-Oxidative Ability.[Pubmed:28328867]
Med Sci Monit. 2017 Mar 22;23:1413-1420.
BACKGROUND Astragaloside IV (AS-IV) has been shown to prevent ischemia-induced acute kidney injury (AKI) in rat models of ischemia and reperfusion. However, the effects of AS-IV on AKI during sepsis and endotoxinemia is unclear. The current study aimed to investigate the effects and molecular mechanisms of AS-IV on lipopolysaccharide (LPS)-induced AKI. MATERIAL AND METHODS Adult male CD-1 mice were randomly assigned into 6 groups (n=8/group): control group: mice were intraperitoneally (i.p.) injected with normal saline; LPS group (10 mg/kg, i.p.); low-dose AS-IV (25 mg/kg; gavage for 7 days) + LPS (i.p., 1 hour after last gavage) group; medial-dose AS-IV (50 mg/kg) + LPS group; high-dose AS-IV (100 mg/kg) + LPS group; high-dose AS-IV alone (100 mg/kg; gavage for 7 days) group. Blood samples were collected at 24 hours after LPS injection, and plasma uric acid and BUN were measured with colorimetric detection kits. The concentration of plasma tumor necrosis factor (TNF)-alpha and interleukin 1beta, renal p-extracellular signal-regulated kinases, and urinary albumin were evaluated by ELISA. The expression of CCR5 in renal tissue was evaluated by PCR and Western blotting. Concentrations of glutathione (GSH) and reactive oxygen species (ROS) in renal tissue were also measured. RESULTS AS-IV decreased LPS-stimulated production of blood TNF-alpha and IL-6, LPS-induced the expression of CCR5, and activation of ERK in the kidneys in a rodent model of endotoxinemia. AS-IV attenuated LPS-caused decreased GSH and increased ROS. It also attenuated LPS-induced increases in plasma uric acid, BUN, and urinary albumin. CONCLUSIONS AS-IV protects against AKI during bacterial endotoxinemia by attenuating expression of cytokines, CCR5, and p-ERK, and elevating anti-oxidative ability.
Astragaloside IV attenuates lead acetate-induced inhibition of neurite outgrowth through activation of Akt-dependent Nrf2 pathway in vitro.[Pubmed:28315454]
Biochim Biophys Acta Mol Basis Dis. 2017 Jun;1863(6):1195-1203.
Recently, oxidative stress is strongly associated with lead (Pb)-induced neurotoxicity. We reported previously that Astragaloside IV (AS-IV) possesses potent antioxidant properties. Here, we evaluate the hypothesis that AS-IV attenuates lead acetate (PbAc)-mediated inhibition of neurite outgrowth might mainly result from its antioxidant property via serine/threonine protein kinase (Akt)-dependent activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Interestingly, AS-IV attenuates PbAc-induced inhibition of neurite outgrowth and displayed potential antioxidant properties by inhibiting reactive oxygen species (ROS). Concomitantly, AS-IV enhanced phase II detoxifying enzymes such as heme oxygenase 1 (HO-1), thioredoxin reductase (TrxR), and glutamate cysteine ligase catalytic subunit (GCLc). Conversely, AS-IV had no effect on GCL modulatory subunit (GCLm) and superoxide dismutase (SOD) activity/expression. Furthermore, AS-IV evoked Akt phosphorylation, and subsequent induced phosphorylation of glycogen synthase kinase-3beta (GSK-3beta) at Ser9 (that is, inactivation), which stimulated Nrf2-mediated antioxidant response element (ARE)-containing activation. Importantly, Akt locates upstream of GSK-3beta and regulates phase II detoxifying enzymes gene expression through Nrf2 nuclear accumulation in PC12 cells exposed to PbAc. Noteworthy, these results were further confirmed through signalling pathway inhibitors, dominant negative mutant and short hairpin RNA technology. Collectively, these in vitro findings suggest that AS-IV attenuates PbAc-induced inhibition of neurite outgrowth attributed to its antioxidant properties and may be a promising candidate for the treatment of lead developmental neurotoxicity.