|Source:||The root of Astragalus membranaceus (Fisch.) Bunge|
|Biological Activity or Inhibitors:||1. Astragaloside IV has been shown to protect the myocardium against ischemia/reperfusion injury, it also has beneficial effect in H/R-induced injury may be related to normalization of SR Ca2+ pump expression and, thus, it may prevent the depression in SR Ca2+ handling.
2. Astragaloside IV can reduce phosphorylation of JNK and ERK1/2 induced by complement membranous attack complex, the mechanism of Astragalus membranaceus in the treatment of membranous nephropathy (MN) may be related to its attenuation of podocyte injury through regulation of cytoskeleton and mitogen activated protein kinase.
3. Astragaloside IV can reduce blood pressure and triglyceride levels in fructose-fed rats and high dose of astragaloside IV also improves glucose tolerance and endothelium-dependent vasorelaxation, it may be useful in ameliorating food-induced metabolic syndrome.
4. Astragaloside IV attenuates inflammatory cytokines by inhibiting TLR4/NF-кB signaling pathway in isoproterenol-induced myocardial hypertrophy, and attenuates Toll-like receptor 4 expression via NF-κB pathway under high glucose condition in mesenchymal stem cells.
5. Astragaloside IV can inhibit adenovirus replication and apoptosis in A549 cells in vitro.
6. Astragaloside IV has anti-fibrotic effect against systemic sclerosis.
|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: firstname.lastname@example.org
|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||1.2739 mL||6.3696 mL||12.7392 mL||25.4784 mL||31.8479 mL|
|5 mM||0.2548 mL||1.2739 mL||2.5478 mL||5.0957 mL||6.3696 mL|
|10 mM||0.1274 mL||0.637 mL||1.2739 mL||2.5478 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|
PLoS One. 2015 Mar 4;10(3):e0118759.
|Astragaloside IV Protects against Isoproterenol-Induced Cardiac Hypertrophy by Regulating NF-κB/PGC-1α Signaling Mediated Energy Biosynthesis.[Pubmed: 25738576]|
|The results showed that combination with Astragaloside IV significantly attenuated the pathological changes, reduced the ratios of heart weight/body weight and Left ventricular weight/body weight, improved the cardiac hemodynamics, down-regulated mRNA expression of Atrial Natriuretic Peptide (ANP) and Brain Natriuretic Peptide (BNP), increased the ratio of ATP/AMP, and decreased the content of Free Fat Acid (FFA) in heart tissue of rats compared with Iso alone. In addition, pretreatment with Astragaloside IV significantly decreased the surface area and protein content, down-regulated mRNA expression of ANP and BNP, increased the ratio of ATP/AMP, and decreased the content of FFA in NRVMs compared with Iso alone. Furthermore, Astragaloside IV increased the protein expression of ATP5D, subunit of ATP synthase and PGC-1α, inhibited translocation of p65, subunit of NF-κB into nuclear fraction in both rats and NRVMs compared with Iso alone. Parthenolide (Par), the specific inhibitor of p65, exerted similar effects as Astragaloside IV in NRVMs. Knockdown of p65 with siRNA decreased the surface areas and increased PGC-1α expression of NRVMs compared with Iso alone. The results suggested that Astragaloside IV protects against Iso-induced cardiac hypertrophy through regulating NF-κB/PGC-1α signaling mediated energy biosynthesis.|
J Cell Mol Med. 2015 Mar 1.
|Remission of CVB3-induced myocarditis with Astragaloside IV treatment requires A20 (TNFAIP3) up-regulation.[Pubmed: 25728713]|
|The results showed that Astragaloside IV administration alleviated the severity of myocarditis and attenuated cardiac inflammation, which was mediated by inhibition of nuclear factor-kappaB (NF-κB) signalling. Importantly, we further identified that the inhibitory effect of Astragaloside IV on NF-κB signalling was through increasing A20 (TNFAIP3) expression. Moreover, we validated that A20 was critical for the therapeutic efficacy of AST-IV on CVB3-induced myocarditis. Finally, we revealed that Astragaloside IV enhanced A20 expression at post-transcriptional level by stabilization of mRNA. Our findings uncover a previously unknown mechanism for Astragaloside IV in the treatment of VMC because of modulating inflammatory response via increasing A20 expression, which provide a potential target for screening new drugs and are helpful for optimization of the therapeutic strategies for VMC.|
Cell Physiol Biochem. 2014;34(6):2105-16.
|Anti-fibrotic effects of Astragaloside IV in systemic sclerosis.[Pubmed: 25562158]|
|Compared to normal fibroblast (NF), the expression of collagen and fibronectin in SSc (SScF) dramatically increased, and this could be reduced by Astragaloside IV (AST) in a dose- or time-dependent manner at both protein and mRNA levels. Administration of Astragaloside IV consistently decreased collagen formation and partially restored the structure, as well as suppressing collagen and fibronectin expression in the skin lesions of SSc-model mice. Mechanistically, Astragaloside IV-induced fibrosis reduction may be due to deregulation of Smad 3/Fli-1, the major mediators of the fibrotic response and key molecules for TGF-β signaling. Astragaloside IV also decreased the level of p-SMAD3 and completely blocked its relocation into the nuclei.|
|Astragaloside IV improved intracellular calcium handling in hypoxia-reoxygenated cardiomyocytes via the sarcoplasmic reticulum Ca-ATPase.[Pubmed: 18349554 ]|
|Astragaloside IV significantly inhibited cardiac troponin I release after H/R in a dose-dependent manner. The diastolic [Ca2+]i measured with Fura-2/AM was significantly increased after reoxygenation. Astragaloside IV prevented the rise of diastolic [Ca2+]i and the depression of caffeine-induced Ca2+ transients caused by H/R. Furthermore, the observed depressions in SR Ca2+-ATPase activity as well as the mRNA and protein expression of SR Ca2+-ATPase in hypoxic-reoxygenated cardiomyocytes were attenuated by Astragaloside IV treatment. These results suggest that the beneficial effect of Astragaloside IV in H/R-induced injury may be related to normalization of SR Ca2+ pump expression and, thus, may prevent the depression in SR Ca2+ handling.|
Phytother Res. 2012 Jun;26(6):892-8.
|Astragaloside IV attenuates complement membranous attack complex induced podocyte injury through the MAPK pathway.[Pubmed: 22086717 ]|
|We found that complement membranous attack complex could increase lactate dehydrogenase (LDH) release from podocytes and Astragaloside IV (AS-IV) could prevent LDH release from podocytes in a time- and dose-dependent pattern. Moreover, AS-IV restored podocyte morphology and cytoskeleton loss induced by complement membranous attack complex. Furthermore, AS-IV was able to reduce phosphorylation of JNK and ERK1/2 induced by complement membranous attack complex. In conclusion, the mechanism of Astragalus membranaceus in the treatment of MN may be related to its attenuation of podocyte injury through regulation of cytoskeleton and mitogen activated protein kinase.|
J Ethnopharmacol. 2013 Dec 12;150(3):1062-70.
|Astragaloside IV attenuates inflammatory cytokines by inhibiting TLR4/NF-кB signaling pathway in isoproterenol-induced myocardial hypertrophy.[Pubmed: 24432369]|
|In vivo: Comparing the Iso group to the control, the HMI, LVMI, TDM were significantly increased; the protein expression of TLR4 and p65 were increased, while the IκBα were decreased; the expression of ANP, TLR4 mRNA, and TNF-α, IL-6 in serum were significantly increased. These changes could be partly prevented by Astragaloside IV and Propranolol. In vitro: the over-expression of the cell size, total protein content could remarkably down-regulated by Astragaloside IV and Propranolol, and the results of RT-PCR, Western blot and ELISA were similar to those of in vivo. CONCLUSIONS: The results of these studies indicate that Astragaloside IV has good protective effect on myocardial hypertrophy induced by isoproterenol. More specifically, the cardioprotection is related to inhibiting the TLR4/NF-кB signaling pathway and the attenuating inflammatory effect.|
J Pharm Pharmacol. 2011 May;63(5):688-94.
|Astragaloside IV inhibits adenovirus replication and apoptosis in A549 cells in vitro.[Pubmed: 21492171 ]|
|TC(0 ) of Astragaloside IV was 116.8 μm, the virus inhibition rate from 15.98% to 65.68% positively was correlated with the concentration of Astragaloside IV from 1.25 μm to 80 μm, IC50 (the medium inhibitory concentration) was 23.85 μm, LC50 (lethal dose 50% concentration) was 865.26 μm and the TI (therapeutic index) was 36.28. qPCR result showed Astragaloside IV inhibited the replication of HAdV-3. Flow FCM analysis demonstrated that the anti-HAdV-3 effect was associated with apoptosis. Astragaloside IV was further detected to reduce the protein expressions of Bax and Caspase-3 and increasing the protein expressions of Bcl-2 using western blotting, which improved the anti-apoptosis mechanism of Astragaloside IV on HAdV-3. CONCLUSIONS: Our findings suggested that Astragaloside IV possessed anti-HAdV-3 capabilities and the underlying mechanisms might involve inhibiting HAdV-3 replication and HAdV-3-induced apoptosis.|