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Astraisoflavan-7-O-β-D-glucoside

$960

  • Brand : BIOFRON

  • Catalogue Number : BD-D0033

  • Specification : HPLC≥98%

  • CAS number : 1011711-05-9

  • Formula : C23H28O11

  • Molecular Weight : 480.466

  • PUBCHEM ID : 134715187

  • Volume : 10mg

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Catalogue Number

BD-D0033

Analysis Method

HPLC,NMR,MS

Specification

HPLC≥98%

Storage

-20℃

Molecular Weight

480.466

Appearance

Powder

Botanical Source

Astragali radix

Structure Type

Category

Standards;Natural Pytochemical;API

SMILES

COC1=C(C(=C(C=C1)C2COC3=C(C2O)C=CC(=C3)OC4C(C(C(C(O4)CO)O)O)O)O)OC

Synonyms

(2S,3R,4S,5S,6R)-2-[[(3R,4R)-4-hydroxy-3-(2-hydroxy-3,4-dimethoxyphenyl)-3,4-dihydro-2H-chromen-7-yl]oxy]-6-(hydroxymethyl)oxane-3,4,5-triol

IUPAC Name

(2S,3R,4S,5S,6R)-2-[[(3R,4R)-4-hydroxy-3-(2-hydroxy-3,4-dimethoxyphenyl)-3,4-dihydro-2H-chromen-7-yl]oxy]-6-(hydroxymethyl)oxane-3,4,5-triol

Applications

Astraganoside, an isoflavane compound, isolated from the roots of Astragalus membranaceus (known as ‘‘Huangqi’’)[1].

Density

Solubility

Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.

Flash Point

Boiling Point

Melting Point

InChl

InChI=1S/C23H28O11/c1-30-14-6-5-11(18(26)22(14)31-2)13-9-32-15-7-10(3-4-12(15)17(13)25)33-23-21(29)20(28)19(27)16(8-24)34-23/h3-7,13,16-17,19-21,23-29H,8-9H2,1-2H3/t13-,16+,17-,19+,20-,21+,23+/m0/s1

InChl Key

JTRBZHFVAAWBNR-IOXUZUKPSA-N

WGK Germany

RID/ADR

HS Code Reference

2933990000

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:1011711-05-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.

PMID

31001851

Abstract

Subjects: The aim of this study was to research the antiapoptotic effect of astragaloside, the principal component of Astragalus membranaceus (Fisch) Bge, in human gingiva cells induced by lipopolysaccharide (LPS).
Methods: According to the treatment, human gingiva cells were divided into five groups, including (1) control group without drug treatment; (2) imitating group, treated with LPS (10 μg·mL-1 ) alone; (3) low group, treated with LPS and 50 μmol·L -1 astragaloside; (4) medium group, treated with LPS and 100 μmol·L -1 astragaloside; and (5) high group, treated with LPS and 150 μmol·L -1 astragaloside. Cell proliferation and apoptosis were investigated using MTT assay and flow cytometry, respectively. Apoptosis and mitogen-activated protein kinase associated proteins were determined using Western blot analysis.
Results: LPS significantly suppressed the proliferation of human gingiva cells, but astragaloside obviously attenuated this change with a dose-dependent manner. LPS significantly promoted the apoptosis of human gingiva cells, but astragaloside treatments significantly attenuated this change with a dose-dependent manner. In addition, LPS could significant upregulated the expression of P-p38, P-JNK, Bax, and caspase-3.
Conclusion: Astragaloside preformed a promising antiapoptotic role in apoptosis of human gingiva cells induced by LPS. This finding might provide us with a novel therapeutic method in tooth protection.

KEYWORDS

apoptosis; astragaloside; gingiva cells; lipopolysaccharide; mitogen-activated protein kinase signaling pathway.

Title

Astragaloside Attenuates Lipopolysaccharide-Induced Cell Apoptosis in Human Gingiva Cells via MAPK Signaling Pathway

Author

Xionghu Shen 1 , Honghua Sun 1 , Hai Cui 1 , Yongmin Jin 1 , Wenbo Jin 1 , Xian Cui 1 , Jie Guo

Publish date

2019 Aug

PMID

29853950

Abstract

Activation of HSC is a pivotal step in hepatic fibrosis. In the activation of HSC, the TGF-β1 plays a key role that can promote the occurrence of hepatic fibrosis by combining with Smad proteins. Astragaloside is the main active component extracted from Radix Astragali that has the effect of antioxidation and hepatoprotection. In the present study, we investigated the mechanism of astragalosides inhibiting hepatic fibrosis in vitro and in vivo. In vitro, astragalosides inhibited the activation of HSC and regulated the expression of MMP-2 and TIMP-2 and reduced the formation of collagen fibers. In vivo, administration of astragalosides decreased the serum ALT, AST, and TBiL in rats by reducing oxidative stress. Astragalosides also attenuated hepatic fibrosis by reducing the concentration of hydroxyproline and inhibiting the formation of collagen fibers. The expressions of TGF-β1, TβR-I, p-Smad 2, and p-Smad 3 were downregulated after astragalosides treatments, while Smad 7 was upregulated compared to the control group. The results indicated that the effect of astragaloside on hepatic fibrosis was related to the inhibition of HSC activation and the modulation of the TGF-β1/Smad signaling pathway.

Title

Astragaloside Inhibits Hepatic Fibrosis by Modulation of TGF- β 1/Smad Signaling Pathway

Author

Xingxing Yuan 1 , Zhiqiang Gong 2 , Bingyu Wang 1 , Xueying Guo 3 , Lei Yang 1 , Dandan Li 1 , Yali Zhang 1

Publish date

2018 Apr 30

PMID

29399127

Abstract

Astragaloside is a monomer isolated from Astragalus membranaceus, a flowering plant in the family Fabaceae. The aim of the present study was to investigate the anti-apoptotic affect of astragaloside on myocardial cells through the TLR4/NF-κB signaling pathway. Astragaloside, NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) and Toll-like receptor 4 (TLR4) blocking antibody solution were prepared in vitro, and myocardial cells were incubated and cultured in serum-free medium overnight. Cells were divided into five groups: the normal control group, serum-free group, astragaloside group, TLR4 blocking antibody group and NF-κB inhibitor PDTC group. The myocardial cell apoptosis in each group was detected using flow cytometry, and the expression levels of TLR4 and NF-κB were detected via western blotting. The apoptosis rate in the serum-free group was significantly higher than that in the normal control group. The apoptosis rate of myocardial cells in the TLR4 blocking antibody group and NF-κB inhibitor PDTC group was lower than that in the serum-free group. In addition, the myocardial cell apoptosis was more obviously decreased in the astragaloside group, and the protein expression levels of TLR4 and NF-κB in the serum-free group were significantly higher than those in normal control group. The protein expression levels of TLR4 and NF-κB in the astragaloside group were obviously lower than those in the serum-free group, and the protein expression levels of TLR4 and NF-κB in the TLR4 blocking antibody group and NF-κB inhibitor PDTC group were decreased. In conclusion, astragaloside reduced myocardial cell apoptosis and protected myocardial cells, which may be one of the mechanisms of a traditional Chinese medicine monomer in treating heart failure.

KEYWORDS

NF-κB; TLR4; astragaloside; myocardial cells.

Title

Astragaloside Protects Myocardial Cells From Apoptosis Through Suppression of the TLR4/NF-κB Signaling Pathway

Author

Yang Zhao 1 , Zhongfen Liu 2 , Hu Zhang 3

Publish date

2018 Feb