We Offer Worldwide Shipping
Login Wishlist

AstragalosideⅡ

$198

  • Brand : BIOFRON

  • Catalogue Number : BF-A3031

  • Specification : 98%

  • CAS number : 84676-89-1

  • Formula : C43H70O15

  • Molecular Weight : 827.01

  • PUBCHEM ID : 158692

  • Volume : 25mg

In stock

Quantity
Checkout Bulk Order?

Catalogue Number

BF-A3031

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

-20℃

Molecular Weight

827.01

Appearance

White crystalline powder

Botanical Source

Astragalus membranaceus,Astragalus membranaceus var. mongholicus

Structure Type

Terpenoids

Category

Standards;Natural Pytochemical;API

SMILES

Synonyms

β-D-Glucopyranoside, (3β,6α,16β,20R,24S)-3-[(2-O-acetyl-β-D-xylopyranosyl)oxy]-20,24-epoxy-16,25-dihydroxy-14-methyl-9,19-cyclocholestan-6-yl/Cyclosieversioside D/(3β,6α,16β,20R,24S)-3-[(2-O-Acetyl-β-D-xylopyranosyl)oxy]-16,25-dihydroxy-14-methyl-20,24-epoxy-9,19-cyclocholestan-6-yl β-D-glucopyranoside/AstrasieversianinVIII/16,25-dihydroxy-9,19-cyclolanostan-6-yl/Astragaloside B/Cyclosiversioside D

IUPAC Name

Density

1.4±0.1 g/cm3

Solubility

Methanol; DMSO

Flash Point

265.3±27.8 °C

Boiling Point

896.9±65.0 °C at 760 mmHg

Melting Point

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2932900000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:84676-89-1) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

28266023

Abstract

OBJECTIVES:
Inhibition of autophagy has been increasingly recognized as a potential therapeutic approach against cancer. Our previous reports showed that Astragaloside II improves hepatic cancer cells resistance by downregulating MDR1 and P-gp .The purpose of this study was to further investigated the effect of autophagy on AS-II reversing multidrug resistance and its molecular mechanism in hepatocellular carcinoma cells in vitro.

METHODS:
Bel-7402 and Bel-7402/FU cell lines were used in this study. Western blot was used to detect the expression of autophagy-related protein, p-mTOR and p-p79s6k, MTT was used to analyse cell viability, GFP-LC3 punctate dots distribution was observed by GFP-LC3 transient transfection under fluorescence microscopy and silencing of autophagy-related genes was detected by small interfering RNA transfection.

KEY FINDINGS:
Astragaloside II was able to significantly decrease the expression of LC3-II and Beclin-1 in a dose-dependent manner, Astragaloside II (80 μm) further decreased LC3-II formation, Beclin-1 and GFP-LC3 puncta dots stimulated with 5-fluorouracil (0.2 mm) in Bel-7402/FU cells (P < 0.05). In addition, Astragaloside II is capable of sensitizing cells to 5-fluorouracil-induced cell death via inhibition of pro-survival autophagy involvement of MAPK-mTOR pathway.

CONCLUSIONS:
These findings suggested that Astragaloside II could suppress autophagy by interfering with Beclin-1 and LC3 via MAPK-mTOR pathway, through which sensitized human cancer resistant cells to 5-FU-induced cell death.

© 2017 Royal Pharmaceutical Society.

KEYWORDS

Astragaloside II; MAPK-mTOR; autophagy; sensitization

Title

Astragaloside II sensitizes human hepatocellular carcinoma cells to 5-fluorouracil via suppression of autophagy.

Author

Wang M1, Huang C2, Su Y1, Yang C3, Xia Q1, Xu DJ1.

Publish date

2017 Jun

PMID

31814910

Abstract

BACKGROUND:
Ulcerative colitis (UC) is a chronic inflammatory intestinal disease, and its morbidity is rising worldwide. Previous study indicated that astragaloside II (AS II), a monomeric compound, was used to treat bowel disease. However, the effects of AS II on UC remains unclear. Thus, this study aimed to investigate the therapeutic effects of AS II on experimental UC in vitro and in vivo.

METHODS:
CCD-18Co cells were stimulated by 1 μg/mL LPS to mimic UC in vitro. In addition, dextran sulfate sodium (DSS)-induced UC mouse model was established in vivo. CCK-8 assay was used to detect cell proliferation in vitro. Moreover, the concentrations of inflammatory factors interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin 1β (IL-1β), nitric oxide (NO), superoxide dismutase (SOD) and malondialdehyde (MDA) in CCD-18Co cells and colon tissues were determined by ELISA, respectively. Meanwhile, the expressions of hypoxia-inducible factor 1α (HIF-α), phospho-inhibitor of NF-κB (p-IκB) and phospho-NF-κB p65 (p-p65) were detected by western blotting in vitro and in vivo, respectively.

RESULTS:
In this study, the levels of pro-inflammatory cytokines TNF-α, IL-1β and IL-6 were significantly increased in lipopolysaccharide (LPS)-stimulated CCD-18Co cells. However, LPS-induced inflammatory response was markedly alleviated by AS II. In addition, LPS-induced HIF-α, p-IκB and p-p65 proteins increases were markedly ameliorated by AS II treatment. Moreover, AS II reduced disease activity index (DAI) scores and increased the colon lengths in DSS-treated mice. Meanwhile, AS II decreased the levels of IL-6, TNF-α, IL-1β, NO, MPO and MDA, and increased the level of SOD in colon of DSS-treated mice. Furthermore, AS II downregulated the expressions of HIF-α, p-IκB and p-p65 in DSS-induced UC in mice.

CONCLUSION:
Our findings indicated that AS II could alleviate inflammatory response in LPS-induced CCD-18Co cells and in DSS-induced UC in mice. In conclusion, AS II may serve as a potential agent for the treatment of UC.

AJTR Copyright © 2019.

KEYWORDS

Astragaloside II; dextran sulfate sodium; lipopolysaccharide; ulcerative colitis

Title

Astragaloside II alleviates the symptoms of experimental ulcerative colitis in vitro and in vivo.

Author

Qiao C1, Wan J2, Zhang L1, Luo B3, Liu P1, Di A1, Gao H1, Sun X1, Zhao G1.

Publish date

2019 Nov 15

PMID

28951595

Abstract

Astragaloside II (AS II) extracted from Astragalus membranaceus has been reported to promote tissue wound repair. However, the effect of AS II on inflammatory bowel disease is unknown. We investigated the effects and mechanism of AS II on intestinal wound healing in both in vitro and in vivo models. Human intestinal Caco-2 cells were treated with multiple concentrations of AS II to assess cell proliferation, scratch wound closure, L-arginine uptake, cationic amino acid transporter activity, and activation of the mTOR signaling pathway. These effects were also measured in a mouse model of colitis. AS II promoted wound closure and increased cell proliferation, L-arginine uptake, CAT1 and CAT2 protein levels, total protein synthesis, and phosphorylation of mTOR, S6K, and 4E-BP1 in Caco-2 cells. These effects were suppressed by lysine or rapamycin treatment, suggesting that the enhanced arginine uptake mediates AS II-induced wound healing. Similar results were also observed in vivo. Our findings indicate that AS II can contribute to epithelial barrier repair following intestinal injury, and may offer a therapeutic avenue in treating irritable bowel disease.

Title

Astragaloside II promotes intestinal epithelial repair by enhancing L-arginine uptake and activating the mTOR pathway.

Author

Lee SY1, Tsai WC2, Lin JC3, Ahmetaj-Shala B4, Huang SF2, Chang WL5, Chang TC6,7,8.

Publish date

2017 Sep 26


Description :

Astragaloside II is a natural isolated from Astragalus.IC50 value:Target:In vitro:In vivo: The developed and validated method has been successfully applied to the quantification and pharmacokinetic study of AST II in rats after intravenous and oral administration of AST II. The oral absolute bioavailability (F) of AST II was calculated to be 0.79 ± 0.16% with an elimination half-life (t1/2) value of 1.92 ± 0.30 h, suggesting its poor absorption and/or strong metabolism in vivo [1].