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Atractylenolide I

$113

  • Brand : BIOFRON

  • Catalogue Number : BF-A2014

  • Specification : 98%

  • CAS number : 73069-13-3

  • Formula : C15H18O2

  • Molecular Weight : 230.3

  • PUBCHEM ID : 5321018

  • Volume : 20mg

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Catalogue Number

BF-A2014

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

-20℃

Molecular Weight

230.3

Appearance

Off-white crystalline powder

Botanical Source

Atractylodes macrocephala

Structure Type

Terpenoids

Category

Standards;Natural Pytochemical;API

SMILES

CC1=C2CC3C(=C)CCCC3(C=C2OC1=O)C

Synonyms

Naphtho[2,3-b]furan-2(4H)-one, 4a,5,6,7,8,8a-hexahydro-3,8a-dimethyl-5-methylene-, (4aS,8aS)-/(4aS,8aS)-3,8a-Dimethyl-5-methylene-4a,5,6,7,8,8a-hexahydronaphtho[2,3-b]furan-2(4H)-one/Atractylenolide-1

IUPAC Name

(4aS,8aS)-3,8a-dimethyl-5-methylidene-4a,6,7,8-tetrahydro-4H-benzo[f][1]benzofuran-2-one

Density

1.1±0.1 g/cm3

Solubility

Methanol; Acetontrile; Dimethylsulfoxide

Flash Point

170.8±25.9 °C

Boiling Point

405.0±44.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C15H18O2/c1-9-5-4-6-15(3)8-13-11(7-12(9)15)10(2)14(16)17-13/h8,12H,1,4-7H2,2-3H3/t12-,15+/m0/s1

InChl Key

ZTVSGQPHMUYCRS-SWLSCSKDSA-N

WGK Germany

RID/ADR

HS Code Reference

2938900000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:73069-13-3) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

28274716

Abstract

Pathogenesis of atherosclerosis is characterized by the proliferation and migration of vascular smooth muscle cells (VSMCs) and inflammatory lesions. The aim of this study is to elucidate the effect of atractylenolide I (AO-I) on smooth muscle cell inflammation, proliferation and migration induced by oxidized modified low density lipoprotein (Ox-LDL). Here, We found that atractylenolide I inhibited Ox-LDL-induced VSMCs proliferation and migration in a dose-dependent manner, and decreased the production of inflammatory cytokines and the expression of monocyte chemoattractant protein-1 (MCP-1) in VSMCs. The study also identified that AO-I prominently inhibited p38-MAPK and NF-κB activation. More importantly, the specific heme oxygenase-1 (HO-1) inhibitor zinc protoporphyrin (ZnPP) IX partially abolished the beneficial effects of atractylenolide I on Ox-LDL-induced VSMCs. Furthermore, atractylenolide I blocked the foam cell formation in macrophages induced by Ox-LDL. In summary, inhibitory roles of AO-I in VSMCs proliferation and migration, lipid peroxidation and subsequent inflammatory responses might contribute to the anti-atherosclerotic property of AO-I.

Copyright © 2017 Elsevier Inc. All rights reserved.

KEYWORDS

Atherosclerosis; Atractylenolide I; Inflammation; Migration; Proliferation; Vascular smooth muscle cells

Title

Atractylenolide I restores HO-1 expression and inhibits Ox-LDL-induced VSMCs proliferation, migration and inflammatory responses in vitro.

Author

Li W1, Zhi W2, Liu F2, He Z2, Wang X2, Niu X3.

Publish date

2017 Apr 1

PMID

32273843

Abstract

Colorectal cancer (CRC) is the third most common cancer worldwide and is associated with a poor clinical outcome and survival. Therefore, the development of novel therapeutic agents for CRC is imperative. Atractylenolide I (AT-I) is a sesquiterpenoid lactone derivative of Rhizoma Atractylodis macrocephalae that exhibits diverse biological activities, including anti-cancer activities. However, the effects and potential mechanism of AT-I in CRC have yet to be fully elucidated. In this study, we aimed to examine the anti-cancer properties of AT-I and the associated functional mechanisms in vitro and in vivo. We found that AT-I treatment significantly suppressed the viability of CRC cell lines and inhibited colony formation, but to a lesser extent in NCM460 cells. Annexin V/PI staining showed that AT-I induced apoptosis in CRC cells, accompanied by increased caspase-3 and PARP-1 cleavage, enhanced expression of Bax, and reduced expression of Bcl-2. Furthermore, AT-I blocked cell glycolysis by inhibiting both glucose uptake and lactate production in CRC cells, and specifically downregulated the expression of the rate-limiting glycolytic enzyme HK2. In contrast, it had no discernable effects on the glycolytic enzymes PFK and PKM2. A mechanistic study revealed that AT-1 negatively regulates STAT3 phosphorylation through direct interaction with JAK2, thereby inhibiting its activation. Moreover, restoring the expression of STAT3 reversed the effect of AT-I on apoptosis and glycolysis in CRC cells. In vivo results revealed that AT-I significantly suppressed tumor growth in HCT116-xenografted mice. Collectively, our findings indicate that the anti-cancer activity of AT-I in CRC is associated with the induction of apoptosis and suppression of glycolysis in CRC cells, via the disruption of JAK2/STAT3 signaling. Our preliminary experimental data indicate that AT-I may have applications as a promising candidate for the treatment of CRC.

Copyright © 2020 Li, Wang, Liu, Guo, Miao and Ma.

KEYWORDS

JAK2; STAT3; apoptosis; atractylenolide I; colorectal cancer; glycolysis

Title

Atractylenolide I Induces Apoptosis and Suppresses Glycolysis by Blocking the JAK2/STAT3 Signaling Pathway in Colorectal Cancer Cells.

Author

Li Y1, Wang Y1, Liu Z1, Guo X1, Miao Z2, Ma S1.

Publish date

2020 Mar 26

PMID

32027273

KEYWORDS

OBJECTIVE:To investigate the effect of atractylenolide I on proliferation and apoptosis of U266 cells, and anti-multiple myeloma effect of bortezomib.METHODS:Bortezomib, bortezomib combined atractylenolide I and atractylenolide I at different concentrations were added into U266 cells respectively, cellular proliferation toxicity was evaluated by CCK-8 assay, apoptosis and cell cycle were detected by using flow cytometry with Annexin V-FITC/PI staining. RT-PCR and Western blot analysis were used to detect the mRNA and protein levels of targeting gene Caspase-3,Caspase-9,BCL-2,BAX,JAK2,STAT3 and IL-6, respectively.RESULTS:The proliferation of U266 cells could inhibited by atractylenolide I, and the apoptosis of U266 cells could be promoted by atractylenolide I, also, which showed a dose-dependent manner(P<0.00; r=0.99). Moreover, the atractylenolide I could regulat the mitochondrial pathway(P<0.01). The combination of 2 drugs could strengther the inhibition of U266 cell proliferation significantly, and the expression level of IL-6,JAK2,STAT3 and BCL-2 mRNA and protein could be decreased by single drug and 2 drugs both(P<0.01).CONCLUSION:Atractylenolide I significantly inhibits the proliferation of U266 cells and promotes their apoptosis. At the same time, it acts synergistically with bortezomib, which may be related to mitochondrial pathway, and probably related to the regulating of IL-6, JAK2 and STAT3 gene expression in signal pathway of JAK2/STAT3.

Title

[Atractylenolide I Can Induce Apoptosis of U266 Cells and Enhance Bortezomib Effect].

Author

Mai ZX1, Yu TQ2, Fan TT1.

Publish date

2020 Feb


Description :

Atractylenolide I is a sesquiterpene derived from the rhizome of Atractylodes macrocephala, possesses diverse bioactivities, such as neuroprotective, anti-allergic, anti-inflammatory and anticancer properties. Atractylenolide I reduces protein levels of phosphorylated JAK2 and STAT3 in A375 cells, and acts as a TLR4-antagonizing agent.