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Atractylodin

$113

  • Brand : BIOFRON

  • Catalogue Number : BF-A3016

  • Specification : 98%

  • CAS number : 55290-63-6

  • Formula : C13H10O

  • Molecular Weight : 182.22

  • PUBCHEM ID : 5321047

  • Volume : 25mg

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Catalogue Number

BF-A3016

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

-20℃

Molecular Weight

182.22

Appearance

White crystalline powder

Botanical Source

Atractylodes lancea

Structure Type

Others

Category

Standards;Natural Pytochemical;API

SMILES

CC=CC#CC#CC=CC1=CC=CO1

Synonyms

I07-0274/2-[(1E,7E)-1,7-Nonadiene-3,5-diyn-1-yl]furan/Atractylodin/2-[(1E,7E)-Nona-1,7-diene-3,5-diyn-1-yl]furan/Furan, 2-(1,7-nonadiene-3,5-diynyl)-, (E,E)-/O921/(E,E)-2-(1,7-Nonadiene-3,5-diynyl)furan/Furan, 2-[(1E,7E)-1,7-nonadiene-3,5-diyn-1-yl]-

IUPAC Name

2-[(1E,7E)-nona-1,7-dien-3,5-diynyl]furan

Density

1.1±0.1 g/cm3

Solubility

Methanol; Ethyl Acetate; Petroleum ether

Flash Point

142.6±12.5 °C

Boiling Point

305.5±34.0 °C at 760 mmHg

Melting Point

InChl

InChl Key

GRBKWAXRYIITKG-QFMFQGICSA-N

WGK Germany

RID/ADR

HS Code Reference

2932190000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:55290-63-6) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

27598116

Abstract

Atractylodin is one of the major constituents of the rhizome of Atractylodes lancea, which is widely used in Korean traditional medicine as a remedy for the treatment of gastritis and gastric ulcers. Despite of a major constituent of widely used botanical to treat inflammatory responses little is known about anti-inflammatory effect of atractylodin in the human mast cell (HMC-1). Hence, we evaluated the effect of atractylodin on the release of IL-6, the involvement of nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) and mitogen-activated protein kinases (MAPKs) in phorbol-12-myristate-13-acetate and A23187-induced HMC-1. In addition, Janus kinase 2 (JAK2), signal transducer and activator of transcription 3 (STAT3), phospholipase C (PLC) gamma 1, and AKT phosphorylation relevant to NPM-ALK signal pathway were assessed. IL-6 levels in the HMC-1 stimulated by phorbol-12-myristate-13-acetate and A23187 were apparently decreased by the treatment of atractylodin. Concurrently, atractylodin not only inhibited the phosphorylation of NPM-ALK, but also suppressed the phosphorylation of JAK2, STAT3, PLC gamma 1, and AKT. Furthermore, the activated mitogen-activated protein kinases (MAPKs) by phorbol-12-myristate-13-acetate and A23187 were inhibited by atractylodin. These results suggested that atractylodin might have a potential regulatory effect on inflammatory mediator expression through blockade of both the phosphorylation of MAPKs and the NPM-ALK signaling pathway.

KEYWORDS

Atractylodes lancea; atractylodin; human mast cell-1; interleukin-6; nucleophosmin-anaplastic lymphoma kinase

Title

Atractylodin Inhibits Interleukin-6 by Blocking NPM-ALK Activation and MAPKs in HMC-1.

Author

Chae HS1, Kim YM2, Chin YW3.

Publish date

2016 Sep 2

PMID

31154759

Abstract

The aim of this study was to evaluate the immunomodulatory effects of atractylodin, a polyethylene alkyne, on the maturation of bone marrow-derived dendritic cells (BM-DC) as well as its antirheumatic effect on collagen-induced arthritis (CIA) in DBA/1 mice. Our results indicate that atractylodin effectively suppressed the secretion of pro-inflammatory cytokines, expression of costimulatory molecules, and p38 MAPK, ERK, and NF-κBp65 signaling pathways in LPS-incubated dendritic cells (DCs). Additionally, the proliferation and cytokine secretion (IFN-γ and IL-17A) of CD8+ and CD4+ T cells were reduced. In a murine CIA model, intraperitoneal injection of atractylodin significantly alleviated the severity of the disease progression, as indicated by reduced paw swelling, clinical arthritis scores, and pathological changes of joint tissues. In addition, the overall proliferation of T cells stimulated by type II collagen and the abundance of Th1 and Th17 in the spleens were also significantly decreased with atractylodin treatments. Furthermore, atractylodin significantly downregulated the expression levels of CD40, CD80, and CD86 of DCs in the spleens. In conclusion, this study shows for the first time that atractylodin has potential to manipulate the maturation of BM-DCs and should be further explored as a therapeutic agent in the treatment of rheumatoid arthritis (RA).

KEYWORDS

T cells; atractylodin; collagen-induced arthritis; dendritic cells; maturation

Title

Atractylodin Suppresses Dendritic Cell Maturation and Ameliorates Collagen-Induced Arthritis in a Mouse Model.

Author

Chuang CH1, Cheng YC1,2, Lin SC3, Lehman CW3, Wang SP4, Chen DY5, Tsai SW6,7, Lin CC1,8,9.

Publish date

2019 Jun 19

PMID

28066135

Abstract

ntestinal disorders often co-occur with inflammation and dysmotility. However, drugs which simultaneously improve intestinal inflammation and co-occurring dysmotility are rarely reported. Atractylodin, a widely used herbal medicine, is used to treat digestive disorders. The present study was designed to characterize the effects of atractylodin on amelioration of both jejunal inflammation and the co-occurring dysmotility in both constipation-prominent (CP) and diarrhea-prominent (DP) rats. The results indicated that atractylodin reduced proinflammatory cytokines TNF-α, IL-1β, and IL-6 in the plasma and inhibited the expression of inflammatory mediators iNOS and NF-kappa B in jejunal segments in both CP and DP rats. The results indicated that atractylodin exerted stimulatory effects and inhibitory effects on the contractility of jejunal segments isolated from CP and DP rats respectively, showing a contractile-state-dependent regulation. Atractylodin-induced contractile-state-dependent regulation was also observed by using rat jejunal segments in low and high contractile states respectively (5 pairs of low/high contractile states). Atractylodin up-regulated the decreased phosphorylation of 20 kDa myosin light chain, protein contents of myosin light chain kinase (MLCK), and MLCK mRNA expression in jejunal segments of CP rats and down-regulated those increased parameters in DP rats. Taken together, atractylodin alleviated rat jejunal inflammation and exerted contractile-state-dependent regulation on the contractility of jejunal segments isolated from CP and DP rats respectively, suggesting the potential clinical implication for ameliorating intestinal inflammation and co-occurring dysmotility.

KEYWORDS

Atractylodin; Constipation; Contractile-state-dependent regulation; Diarrhea; Inflammation; Jejunal contractility

Title

Ameliorative effects of atractylodin on intestinal inflammation and co-occurring dysmotility in both constipation and diarrhea prominent rats.

Author

Yu C1, Xiong Y1, Chen D1, Li Y1, Xu B1, Lin Y1, Tang Z1, Jiang C1, Wang L1.

Publish date

2017 Jan


Description :

Atractylodin is an active component of the essential oil contained in the rhizomes of Atractylodes lancea and A.