1. Metabolic Enzyme/Protease
    Stem Cell/Wnt
    MAPK/ERK Pathway
  2. MMP
    ERK
    JNK
  3. Astragaloside IV

Astragaloside IV 

Cat. No.: HY-N0431 Purity: >98.0%
Handling Instructions

Astragaloside IV, an active component isolated from Astragalus membranaceus, suppresses the activation of ERK1/2 and JNK, and downregulates matrix metalloproteases (MMP)-2, (MMP)-9 in MDA-MB-231 breast cancer cells.

For research use only. We do not sell to patients.

Astragaloside IV Chemical Structure

Astragaloside IV Chemical Structure

CAS No. : 84687-43-4

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10 mM * 1  mL in DMSO USD 66 In-stock
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100 mg USD 288 In-stock
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Customer Review

Based on 5 publication(s) in Google Scholar

Top Publications Citing Use of Products

    Astragaloside IV purchased from MCE. Usage Cited in: Front Pharmacol. 2018 Apr 16;9:345.

    AMP-activated protein kinase activation by AST inhibits the expression of sterol regulatory element binding protein-1c (SREBP-1c) and SREBP-1c related genes. AST promotes AMPKa1 mRNA expression, AMPKa2 mRNA expression, and suppresses the expression of SREBP-1c, and its downstream genes FAS, ACC1, and also AMPK downstream gene SCD1.

    Astragaloside IV purchased from MCE. Usage Cited in: Front Pharmacol. 2018 Apr 16;9:345.

    AMP-activated protein kinase (AMPK) activation by AST blunts dysfunction of lipid metabolism and insulin resistance in HepG2 cells. Representative bands of SREBP-1c nuclear protein and cytoplasmic proteins are visualized in the immunoblotting assay.

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    • Biological Activity

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    • References

    • Customer Review

    Description

    Astragaloside IV, an active component isolated from Astragalus membranaceus, suppresses the activation of ERK1/2 and JNK, and downregulates matrix metalloproteases (MMP)-2, (MMP)-9 in MDA-MB-231 breast cancer cells.

    IC50 & Target[4]

    MMP-2

     

    MMP-9

     

    ERK1

     

    ERK2

     

    JNK

     

    In Vitro

    Astragaloside IV (10, 20, 40 ng/mL) inhibits NSCLC cell growth, whereas low concentrations of astragaloside IV (1, 2.5, 5 ng/mL) has no obvious cytotoxicity on cell viability. Moreover, combined treatment with astragaloside IV significantly increases chemosensitivity to cisplatin in NSCLC cells. On the molecular level, astragaloside IV co-treatment significantly inhibits the mRNA and protein levels of B7-H3 in the presence of cisplatin[2]. Astragaloside IV inhibits the viability and invasive potential of MDA-MB-231 breast cancer cells, suppresses the activation of the mitogen activated protein kinase (MAPK) family members ERK1/2 and JNK, and downregulates matrix metalloproteases (MMP)-2 and -9[4].

    In Vivo

    Astragaloside IV (10, 20 mg/kg, p.o.) exhibits a potent ability to prevent cognitive deficits induced by transient cerebral ischemia and reperfusion. Astragaloside IV (10 mg/kg) and Astragaloside IV (20 mg/kg) can significantly decrease the levels of these cytokines compared to the Model group. Astragaloside IV significantly inhibits the level of TLR4 and its downstream proteins, suggesting that both MyD88-dependent and -independent pathways play important roles in the anti-inflammatory effects of Astragaloside IV. Astragaloside IV attenuates NLRP3 and cleaved-caspase-1 expression, and reduces Iba1 protein expression[1]. In the mice model, the high-dose astragaloside IV group has a significant increase in the 48-hour survival rate [60% (9/15) vs 13.3% (2/15), P < 0.05], significant reductions in the serum ALT and AST levels (P < 0.01), and significant reductions in liver histopathological indices and the degree of apoptosis of hepatocytes (P < 0.01), as well as a significant reduction in the content of MDA in liver homogenate (P < 0.01) and a significant increase in the activity of SOD[3].

    Molecular Weight

    784.97

    Formula

    C₄₁H₆₈O₁₄

    CAS No.

    84687-43-4

    SMILES
    Shipping

    Room temperature in continental US; may vary elsewhere.

    Storage
    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month
    Solvent & Solubility
    In Vitro: 

    DMSO : ≥ 100 mg/mL (127.39 mM)

    *"≥" means soluble, but saturation unknown.

    Preparing
    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 1.2739 mL 6.3697 mL 12.7393 mL
    5 mM 0.2548 mL 1.2739 mL 2.5479 mL
    10 mM 0.1274 mL 0.6370 mL 1.2739 mL
    *Please refer to the solubility information to select the appropriate solvent.
    In Vivo:
    • 1.

      Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

      Solubility: 2.5 mg/mL (3.18 mM); Suspended solution; Need ultrasonic

    • 2.

      Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in saline)

      Solubility: ≥ 2.5 mg/mL (3.18 mM); Clear solution

    • 3.

      Add each solvent one by one:  10% DMSO    90% corn oil

      Solubility: ≥ 2.5 mg/mL (3.18 mM); Clear solution

    *All of the co-solvents are provided by MCE.
    References
    Kinase Assay
    [4]

    Briefly, MDA-MB-231 cells treated as indicated or tumor tissues are harvested and lysed in Mg2+ lysis buffer containing 50 mM Tris (pH 7.5), 10 mM MgCl2, 0.5 M NaCl, and protease inhibitor cocktail. Equal amounts of lysates are incubated with PAK-PBD beads at 4°C for 1 h. PAK-PBD beads are pelleted by centrifugation and washed with ish buffer containing 25 mM Tris (pH 7.5), 30 mM MgCl2, 40 mM NaCl. Active Rac1 is detected by western blotting.

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Cell Assay
    [2]

    Cell viability is determined by CCK-8 assay. To be brief, cultured NSCLC cells are seeded into 96-well plates at the density of 4×104 (cells/well). Then 10 µL⁄well CCK8 solution is added and incubated in dark at 37°C for another 2 h. The absorbance is determined with the wavelength of 490 nm.

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Administration
    [1]

    Transient cerebral ischemia and reperfusion is prepared by BCCAO, as BCCAO is considered an ideal model to study transient cerebral ischemia and reperfusion injury-mediated inflammatory response. Mice are randomLy divided into the Sham, Model, Astragaloside IV (10 mg/kg) and Astragaloside IV (20 mg/kg) treatment groups. The Astragaloside IV treatment groups are intragastrically administered 7 days before the surgery and terminated on the day of sacrifice. On the day of the surgery, Astragaloside IV is administrated 2 h prior to ischemia. The Sham-operated and Model groups are treated with distilled water. After the mice are anesthetized with an intraperitoneal injection of chloral hydrate (350 mg/kg), the bilateral common carotid arteries are exposed and carefully separated with a small ventral neck incision and occluded twice (20 min each) with ligated surgical silk as described previously with minor modifications. There is a 10 min reperfusion period between the two occlusion periods (ischemia 20 min − reperfusion 10 min − ischemia 20 min). Sham-operated mice are subjected to the same surgical operation without the surgical silk ligation. Mouse body temperature is maintained at 37±0.5°C during the surgery with heating equipment until recovery from the anesthesia.

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    References

    Purity: >98.0%

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    Keywords:

    Astragaloside IVMMPERKJNKMatrix metalloproteinasesExtracellular signal regulated kinasesc-Jun N-terminal kinaseInhibitorinhibitorinhibit

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