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Dieckol

$1,930

  • Brand : BIOFRON

  • Catalogue Number : BN-O1442

  • Specification : 98%(HPLC)

  • CAS number : 88095-77-6

  • Formula : C36H22O18

  • Molecular Weight : 742.5

  • PUBCHEM ID : 3008868

  • Volume : 20mg

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Catalogue Number

BN-O1442

Analysis Method

Specification

98%(HPLC)

Storage

2-8°C

Molecular Weight

742.5

Appearance

Botanical Source

Structure Type

Category

SMILES

C1=C(C=C(C=C1O)OC2=C(C=C(C3=C2OC4=C(C=C(C=C4O3)OC5=C(C=C(C=C5O)OC6=C(C=C(C7=C6OC8=C(C=C(C=C8O7)O)O)O)O)O)O)O)O)O

Synonyms

Dieckol

IUPAC Name

4-[4-[6-(3,5-dihydroxyphenoxy)-4,7,9-trihydroxydibenzo-p-dioxin-2-yl]oxy-3,5-dihydroxyphenoxy]dibenzo-p-dioxin-1,3,6,8-tetrol

Density

Solubility

Flash Point

Boiling Point

Melting Point

InChl

InChl Key

DRZQFGYIIYNNEC-UHFFFAOYSA-N

WGK Germany

RID/ADR

HS Code Reference

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:88095-77-6) 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

31291034

Abstract

Non-small-cell lung cancer (NSCLC) is one of the most prevalent type of lung cancers with an increased mortality rate in both developed and developing countries worldwide. Dieckol is one such polyphenolic drug extracted from brown algae which has proven antioxidant and anti-inflammatory properties. In the present study, we evaluated the anticancer property of dieckol against NSCLC cell line A549. The LC50 value of dieckol was found to be 25 µg/mL by performing 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and the antiapoptotic property of dieckol was analyzed by dual staining technique with acridine orange/propidium iodide (AO/PI) stains. It was further confirmed with flow cytometry analysis with Annexin FITC and JC-1 staining and the anti-invasive property was assessed by Transwell assay. The molecular mechanism of dieckol anticancer activity was confirmed by estimating the levels of caspases and by estimating the signaling proteins of Pi3K/AKT/mTOR signaling pathway using the immunoblotting technique. Our data suggest that dieckol is potent anticancer agent, it effectively inhibits the invasive and migratory property A549 cells and it also induces apoptosis via inhibiting Pi3K/AKT/mTOR signaling, activating the tumor suppressor protein E-cadherin signifying that dieckol is potent natural anticancer drug to treat NSCLC.

© 2019 The Authors. Journal of Biochemical and Molecular Toxicology Published by Wiley Periodicals, Inc.

KEYWORDS

NSCLC; PI3K/AKT/mTOR; anticancer drug; cadherin; dieckol; lung cancer

Title

Dieckol inhibits non-small-cell lung cancer cell proliferation and migration by regulating the PI3K/AKT signaling pathway.

Author

Wang CH1, Li XF1, Jin LF1, Zhao Y1, Zhu GJ1, Shen WZ1.

Publish date

2019 Aug

PMID

25216701

Abstract

PURPOSE:
Ecklonia cava is an abundant brown alga and has been reported to possess various bioactive compounds having anti-inflammatory effect. However, the anticancer effects of dieckol, a major active compound in E. cava, are poorly understood. In the present study, we investigated the anti-tumor activity of dieckol and its molecular mechanism in ovarian cancer cells and in a xenograft mouse model .

METHODS:
MTT assay, PI staining, and PI and Annexin double staining were performed to study cell cytotoxicity, cell cycle distribution, and apoptosis. We also investigated reactive oxygen species (ROS) production and protein expression using flow cytometry and Western blot analysis, respectively. Anti-tumor effects of dieckol were evaluated in SKOV3 tumor xenograft model.

RESULTS:
We found that the E. cava extract and its phlorotannins have cytotoxic effects on A2780 and SKOV3 ovarian cancer cells. Dieckol induced the apoptosis of SKOV3 cells and suppressed tumor growth without any significant adverse effect in the SKOV3-bearing mouse model. Dieckol triggered the activation of caspase-8, caspase-9, and caspase-3, and pretreatment with caspase inhibitors neutralized the pro-apoptotic activity of dieckol. Furthermore, treatment with dieckol caused mitochondrial dysfunction and suppressed the levels of anti-apoptotic proteins. We further demonstrated that dieckol induced an increase in intracellular ROS, and the antioxidant N-acetyl-L-cysteine (NAC) significantly reversed the caspase activation, cytochrome c release, Bcl-2 downregulation, and apoptosis that were caused by dieckol. Moreover, dieckol inhibited the activity of AKT and p38, and overexpression of AKT and p38, at least in part, reversed dieckol-induced apoptosis in SKOV3 cells.

CONCLUSION:
These data suggest that dieckol suppresses ovarian cancer cell growth by inducing caspase-dependent apoptosis via ROS production and the regulation of AKT and p38 signaling.

Title

Dieckol, isolated from the edible brown algae Ecklonia cava, induces apoptosis of ovarian cancer cells and inhibits tumor xenograft growth.

Author

Ahn JH1, Yang YI, Lee KT, Choi JH.

Publish date

2015 Feb

PMID

25944759

Abstract

SCOPE:
Dieckol is a major polyphenol of Ecklonia cava. This study demonstrates a mechanistic role for dieckol in the suppression of lipid accumulation using three models.

METHODS AND RESULTS:
Mice were split into four experimental groups (n = 10 per group): normal diet, high-fat diet (HFD), and dieckol-supplemented diets. Dieckol-supplemented mice groups showed a significant decrease of body weight gain (38%) as well as fats of organs including epididymal (45%) compared with a HFD-fed group. LDL cholesterol level was reduced by 55% in dieckol-supplemented group. Adipogenic factors and lipid synthetic enzymes were analyzed via real-time PCR or immunoblotting. Dieckol regulated mRNA expressions of early adipogenic genes in 3T3-L1 cells. These results were reflected in downregulation of late adipogenic factors, resulting in a decrease in triacylglycerol content. These data were also verified in zebrafish and mouse models. Dieckol activated AMP-activated protein kinase α (AMPKα) signaling to inhibit lipid synthesis in 3T3-L1 and mouse model. Dieckol was also shown to inhibit mitotic clonal expansion via cell-cycle arrest.

CONCLUSION:
Our data demonstrate that dieckol inhibits lipid accumulation via activation of AMPKα signaling and cell-cycle arrest.

© 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

KEYWORDS

3T3-L1; Adipogenesis; Dieckol; Mice; Zebrafish

Title

Dieckol, a major phlorotannin in Ecklonia cava, suppresses lipid accumulation in the adipocytes of high-fat diet-fed zebrafish and mice: Inhibition of early adipogenesis via cell-cycle arrest and AMPKα activation.

Author

Choi HS1, Jeon HJ2, Lee OH3, Lee BY2.

Publish date

2015 Aug


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