Astragaloside IV

CAS# 84687-43-4

Astragaloside IV

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Chemical structure

Astragaloside IV

3D structure

Chemical Properties of Astragaloside IV

Cas No. 84687-43-4 SDF Download SDF
PubChem ID 158694 Appearance White powder
Formula C41H68O14 M.Wt 784.98
Type of Compound Triterpenoids Storage Desiccate at -20°C
Synonyms Astrasieversianin XIV; Astraversianin XIV; Cyclosieversioside F
Solubility DMSO : 390 mg/mL (496.83 mM; Need ultrasonic)
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-CSXKERSZSA-N
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 Astragaloside IV

The root of Astragalus membranaceus (Fisch.) Bunge

Biological Activity of Astragaloside IV

DescriptionAstragaloside IV can protect the myocardium against ischemia/reperfusion injury, inhibit adenovirus replication and apoptosis in A549 cells in vitro, has anti-fibrotic effect against systemic sclerosis, and may be useful in ameliorating food-induced metabolic syndrome and membranous nephropathy. It suppresses the activation of ERK1/2 and JNK, and downregulates matrix metalloproteases (MMP)-2, (MMP)-9 in MDA-MB-231 breast cancer cells.
Targetsp65 | NF-kB | TGF-β/Smad | Calcium Channel | TNF-α | LTR | Bcl-2/Bax | Caspase | IL Receptor | Antifection
In vitro

Astragaloside IV improved intracellular calcium handling in hypoxia-reoxygenated cardiomyocytes via the sarcoplasmic reticulum Ca-ATPase.[Pubmed: 18349554 ]

Pharmacology. 2008;81(4):325-32.

Although Astragaloside IV, a saponin isolated from Astragalus membranaceus, has been shown to protect the myocardium against ischemia/reperfusion injury, its effect on the status of sarcoplasmic reticulum (SR) Ca2+ transport in the injured myocardium remains largely unknown.
METHODS AND RESULTS:
In this study, we investigated whether in cultured cardiomyocytes subjected to hypoxia and reoxygenation (H/R) administration of Astragaloside IV during H/R attenuates the myocardial cell injury and prevents changes in Ca2+ handling activities and gene expression of SR Ca2+ pump. Cultured cardiomyocytes from neonatal rats were exposed to 6 h of hypoxia followed by 3 h of reoxygenation. Myocyte injury was determined by the release of cardiac troponin I in supernatant. 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.
CONCLUSIONS:
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.

Astragaloside IV inhibits adenovirus replication and apoptosis in A549 cells in vitro.[Pubmed: 21492171 ]

J Pharm Pharmacol. 2011 May;63(5):688-94.

Astragaloside IV, purified from the Chinese medical herb Astragalus membranaceus (Fisch) Bge and Astragalus caspicus Bieb, is an important natural product with multiple pharmacological actions. This study investigated the anti-ADVs effect of Astragaloside IV on HAdV-3 (human adenovirus type 3) in A549 cell.
METHODS AND RESULTS:
CPE, MTT, quantitative real-time PCR (qPCR), flow cytometry (FCM) and Western blot were apply to detect the cytotoxicity, the inhibition and the mechanisms of Astragaloside IV on HAdV-3. 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.

In vivo

Astragaloside IV Protects against Isoproterenol-Induced Cardiac Hypertrophy by Regulating NF-κB/PGC-1α Signaling Mediated Energy Biosynthesis.[Pubmed: 25738576]

PLoS One. 2015 Mar 4;10(3):e0118759.

We previously reported that Astragaloside IV (ASIV), a major active constituent of Astragalus membranaceus (Fisch) Bge protects against cardiac hypertrophy in rats induced by isoproterenol (Iso), however the mechanism underlying the protection remains unknown. Dysfunction of cardiac energy biosynthesis contributes to the hypertrophy and Nuclear Factor κB (NF-κB)/Peroxisome Proliferator-Activated Receptor-γ Coactivator 1α (PGC-1α) signaling gets involved in the dysfunction.
METHODS AND RESULTS:
The present study was designed to investigate the mechanism by which ASIV improves the cardiac hypertrophy with focuses on the NF-κB/PGC-1α signaling mediated energy biosynthesis. Sprague-Dawley (SD) rats or Neonatal Rat Ventricular Myocytes (NRVMs) were treated with Iso alone or in combination with ASIV. The results showed that combination with ASIV 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 ASIV 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, ASIV 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 ASIV in NRVMs. Knockdown of p65 with siRNA decreased the surface areas and increased PGC-1α expression of NRVMs compared with Iso alone.
CONCLUSIONS:
The results suggested that ASIV protects against Iso-induced cardiac hypertrophy through regulating NF-κB/PGC-1α signaling mediated energy biosynthesis.

Anti-fibrotic effects of Astragaloside IV in systemic sclerosis.[Pubmed: 25562158]

Cell Physiol Biochem. 2014;34(6):2105-16.

To evaluate the anti-fibrotic effects of Astragaloside IV in systemic sclerosis.
METHODS AND RESULTS:
Treated or untreated systemic sclerosis (SSc) and normal fibroblast isolated from corresponding pairs were utilized to detect expression of collagen and fibronectin by western blot, quantitative real-time RT-PCR (RT-qPCR), immunofluorescence staining and histopathological examination. SSc mouse model induced by bleomycin was used to evaluate the effects of the drug in vivo. 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.
CONCLUSIONS:
Astragaloside IV attenuates fibrosis by inhibiting the TGF-β-Smads3 axis in systemic sclerosis.

Astragaloside IV attenuates complement membranous attack complex induced podocyte injury through the MAPK pathway.[Pubmed: 22086717 ]

Phytother Res. 2012 Jun;26(6):892-8.

Membranous nephropathy (MN) is the most common cause of idiopathic nephrotic syndrome in adults and the cause is known to be due to the injury of podocytes located in the glomeruli. Astragalus membranaceus has been used for the treatment of patients with MN in China for a long time. The beneficial effect of Astragalus membranaceus on proteinuria of patients with MN has been well documented. However, the mechanism of astragalus membranaceu in alleviation of MN is still not completely understood.
METHODS AND RESULTS:
Therefore, in the current study, we employed a podocyte injury model induced by complement membranous attack complex to examine the mechanism of astragalus membraneceus in the treatment of MN. 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.
CONCLUSIONS:
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.

Protocol of Astragaloside IV

Cell Research

Astragaloside IV improves lipid metabolism in obese mice by alleviation of leptin resistance and regulation of thermogenic network.[Pubmed: 27444146]

Sci Rep. 2016; 6: 30190.

Cell lines:SH-SY5Y cells
Concentrations: 0, 25, 50 and 100 μM
Incubation Time: 24 h
Method:
Neuronal cell line SH-SY5Y cells are maintained in DMEM/F-12 medium supplemented with 10% fetal bovine serum (FBS) at 37 °C in a humidified incubator supplied with 5% CO2. After seeded in 6-well plate at 5 × 105 cells/ml and cultured without FBS overnight, the cells are treated with ASI (0, 25, 50 and 100 μM) for 24 h. Thereafter, they are harvested with CelLyticTM MT mammalian tissue lysis reagent supplemented with protease and phosphatase inhibitors followed by sonication, and stored at −80℃ for further western blotting analysis.

Animal Research

Astragaloside IV improves lipid metabolism in obese mice by alleviation of leptin resistance and regulation of thermogenic network.[Pubmed: 27444146]

Sci Rep. 2016; 6: 30190.

Animal Models:Six-weeks old male C57BL/6 mice
Formulation: ---
Dosages:25 mg/kg/d
Administration: i.p.

Astragaloside IV Dilution Calculator

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Preparing Stock Solutions of Astragaloside IV

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
* 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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Background on Astragaloside IV

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.

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].

References:
[1]. Li M, et al. Astragaloside IV attenuates cognitive impairments induced by transient cerebral ischemia and reperfusion in mice via anti-inflammatory mechanisms. Neurosci Lett. 2016 Dec 20. pii: S0304-3940(16)30994-6 [2]. He CS, et al. Astragaloside IV Enhances Cisplatin Chemosensitivity in Non-Small Cell Lung Cancer Cells Through Inhibition of B7-H3. Cell Physiol Biochem. 2016;40(5):1221-1229. Epub 2016 Dec 14. [3]. Liu L, et al. [Protective effect of astragaloside IV against acute liver failure in experimental mice]. Zhonghua Gan Zang Bing Za Zhi. 2016 Oct 20;24(10):772-777. [4]. Jiang K, et al. Astragaloside IV inhibits breast cancer cell invasion by suppressing Vav3 mediated Rac1/MAPK signaling. Int Immunopharmacol. 2016 Dec 5;42:195-202

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References on Astragaloside IV

Astragaloside IV attenuates complement membranous attack complex induced podocyte injury through the MAPK pathway.[Pubmed:22086717]

Phytother Res. 2012 Jun;26(6):892-8.

Membranous nephropathy (MN) is the most common cause of idiopathic nephrotic syndrome in adults and the cause is known to be due to the injury of podocytes located in the glomeruli. Astragalus membranaceus has been used for the treatment of patients with MN in China for a long time. The beneficial effect of Astragalus membranaceus on proteinuria of patients with MN has been well documented. However, the mechanism of astragalus membranaceu in alleviation of MN is still not completely understood. Therefore, in the current study, we employed a podocyte injury model induced by complement membranous attack complex to examine the mechanism of astragalus membraneceus in the treatment of MN. 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.

Astragaloside IV inhibits adenovirus replication and apoptosis in A549 cells in vitro.[Pubmed:21492171]

J Pharm Pharmacol. 2011 May;63(5):688-94.

OBJECTIVES: Astragaloside IV, purified from the Chinese medical herb Astragalus membranaceus (Fisch) Bge and Astragalus caspicus Bieb, is an important natural product with multiple pharmacological actions. This study investigated the anti-ADVs effect of Astragaloside IV on HAdV-3 (human adenovirus type 3) in A549 cell. METHODS: CPE, MTT, quantitative real-time PCR (qPCR), flow cytometry (FCM) and Western blot were apply to detect the cytotoxicity, the inhibition and the mechanisms of Astragaloside IV on HAdV-3. KEY FINDINGS: TC(0 ) of Astragaloside IV was 116.8 microm, the virus inhibition rate from 15.98% to 65.68% positively was correlated with the concentration of Astragaloside IV from 1.25 microm to 80 microm, IC50 (the medium inhibitory concentration) was 23.85 microm, LC50 (lethal dose 50% concentration) was 865.26 microm 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.

Anti-fibrotic effects of Astragaloside IV in systemic sclerosis.[Pubmed:25562158]

Cell Physiol Biochem. 2014;34(6):2105-16.

OBJECTIVE: To evaluate the anti-fibrotic effects of Astragaloside IV in systemic sclerosis. METHODS: Treated or untreated systemic sclerosis (SSc) and normal fibroblast isolated from corresponding pairs were utilized to detect expression of collagen and fibronectin by western blot, quantitative real-time RT-PCR (RT-qPCR), immunofluorescence staining and histopathological examination. SSc mouse model induced by bleomycin was used to evaluate the effects of the drug in vivo. RESULTS: 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-beta signaling. Astragaloside IV also decreased the level of p-SMAD3 and completely blocked its relocation into the nuclei. CONCLUSION: Astragaloside IV attenuates fibrosis by inhibiting the TGF-beta-Smads3 axis in systemic sclerosis.

Astragaloside IV attenuates inflammatory cytokines by inhibiting TLR4/NF-small ka, CyrillicB signaling pathway in isoproterenol-induced myocardial hypertrophy.[Pubmed:24432369]

J Ethnopharmacol. 2013 Dec 12;150(3):1062-70.

ETHNOPHARMACOLOGICAL RELEVANCE: Astragaloside IV (As IV) is one of the main effective components isolated from the traditional Chinese medical herb Astragalus membranaceus. The protective effect of Astragalus membranaceus on myocardial hypertrophy has been extensively proved. To test the hypothesis that Astragaloside IV can ameliorate the myocardial hypertrophy and inflammatory effect induced by beta-adrenergic hyperactivity, we carried out in vivo and in vitro experiments. MATERIAL AND METHODS: In in vivo study, the isoproterenol (Iso) (5 mg kg(-1) d(-1)) was used as a model of myocardial hypertrophy by intraperitoneal injection. SD rats were randomly assigned to following six groups: A: the control; B: Iso group; C: Iso plus As IV 20 mg kg(-1) d(-1); D: Iso plus As IV 40 mg kg(-1) d(-1); E: Iso plus As IV 80 mg kg(-1) d(-1); F: Iso plus Propranolol 40 mg kg(-1) d(-1). In in vitro study, cultured neonatal rat cardiomyocytes were pretreated with As IV (3, 10, 30 mu mol L(-1)), Propranolol (2 mu mol L(-1)) and BAY11-7082 (5 mu mol L(-1)) for 30 min, and then incubated with Iso (10 mu mol L(-1)) for 48 h. For the rats in each group, the heart mass index (HMI) and the left ventricular mass index (LVMI) were measured. To measure the transverse diameter of left ventricular myocardial cells (TDM), the hematoxylin-eosin (HE) staining method was applied. In addition, the volume and the total protein content of cardiomyocytes were measured, the mRNA expression of ANP and TLR4 were quantified by RT-PCR, the protein expression of TLR4, IkappaBalpha and p65 were quantified by Western blot, and the level of TNF-alpha and IL-6 were measured by ELISA. RESULTS: 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 IkappaBalpha were decreased; the expression of ANP, TLR4 mRNA, and TNF-alpha, IL-6 in serum were significantly increased. These changes could be partly prevented by As IV and Pro. In vitro: the over-expression of the cell size, total protein content could remarkably down-regulated by As IV and Pro, 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-small ka, CyrillicB signaling pathway and the attenuating inflammatory effect.

Astragaloside IV protects against isoproterenol-induced cardiac hypertrophy by regulating NF-kappaB/PGC-1alpha signaling mediated energy biosynthesis.[Pubmed:25738576]

PLoS One. 2015 Mar 4;10(3):e0118759.

We previously reported that Astragaloside IV (ASIV), a major active constituent of Astragalus membranaceus (Fisch) Bge protects against cardiac hypertrophy in rats induced by isoproterenol (Iso), however the mechanism underlying the protection remains unknown. Dysfunction of cardiac energy biosynthesis contributes to the hypertrophy and Nuclear Factor kappaB (NF-kappaB)/Peroxisome Proliferator-Activated Receptor-gamma Coactivator 1alpha (PGC-1alpha) signaling gets involved in the dysfunction. The present study was designed to investigate the mechanism by which ASIV improves the cardiac hypertrophy with focuses on the NF-kappaB/PGC-1alpha signaling mediated energy biosynthesis. Sprague-Dawley (SD) rats or Neonatal Rat Ventricular Myocytes (NRVMs) were treated with Iso alone or in combination with ASIV. The results showed that combination with ASIV 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 ASIV 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, ASIV increased the protein expression of ATP5D, subunit of ATP synthase and PGC-1alpha, inhibited translocation of p65, subunit of NF-kappaB into nuclear fraction in both rats and NRVMs compared with Iso alone. Parthenolide (Par), the specific inhibitor of p65, exerted similar effects as ASIV in NRVMs. Knockdown of p65 with siRNA decreased the surface areas and increased PGC-1alpha expression of NRVMs compared with Iso alone. The results suggested that ASIV protects against Iso-induced cardiac hypertrophy through regulating NF-kappaB/PGC-1alpha signaling mediated energy biosynthesis.

Astragaloside IV improved intracellular calcium handling in hypoxia-reoxygenated cardiomyocytes via the sarcoplasmic reticulum Ca-ATPase.[Pubmed:18349554]

Pharmacology. 2008;81(4):325-32.

Although Astragaloside IV, a saponin isolated from Astragalus membranaceus, has been shown to protect the myocardium against ischemia/reperfusion injury, its effect on the status of sarcoplasmic reticulum (SR) Ca2+ transport in the injured myocardium remains largely unknown. In this study, we investigated whether in cultured cardiomyocytes subjected to hypoxia and reoxygenation (H/R) administration of Astragaloside IV during H/R attenuates the myocardial cell injury and prevents changes in Ca2+ handling activities and gene expression of SR Ca2+ pump. Cultured cardiomyocytes from neonatal rats were exposed to 6 h of hypoxia followed by 3 h of reoxygenation. Myocyte injury was determined by the release of cardiac troponin I in supernatant. 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.

Remission of CVB3-induced myocarditis with Astragaloside IV treatment requires A20 (TNFAIP3) up-regulation.[Pubmed:25728713]

J Cell Mol Med. 2015 Apr;19(4):850-64.

Viral myocarditis (VMC) most prevalently caused by coxsackievirus B3 (CVB3) infection is characterized by severe cardiac inflammation. Therapeutic options for the disease are still limited. Astragaloside IV (AST-IV), a purified small molecular saponin (C41 H68 O14 , MW 784), is the main active component of Chinese medical herb Astragalus which has been empirically prescribed for the treatment of heart dysfunction for centuries. In this study, we investigated the effect of AST-IV on CVB3-induced myocarditis and explored its possible mechanism involved. The results showed that AST-IV administration alleviated the severity of myocarditis and attenuated cardiac inflammation, which was mediated by inhibition of nuclear factor-kappaB (NF-kappaB) signalling. Importantly, we further identified that the inhibitory effect of AST-IV on NF-kappaB 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 AST-IV enhanced A20 expression at post-transcriptional level by stabilization of mRNA. Our findings uncover a previously unknown mechanism for AST-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.

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.

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