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Cynaroside

$275

  • Brand : BIOFRON

  • Catalogue Number : BF-C1020

  • Specification : 98%

  • CAS number : 5373-11-5

  • Formula : C21H20O11

  • Molecular Weight : 448.38

  • PUBCHEM ID : 5280637

  • Volume : 20mg

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Catalogue Number

BF-C1020

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

-20℃

Molecular Weight

448.38

Appearance

Yellow crystalline powder

Botanical Source

Chrysanthemum morifolium

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

C1=CC(=C(C=C1C2=CC(=O)C3=C(C=C(C=C3O2)OC4C(C(C(C(O4)CO)O)O)O)O)O)O

Synonyms

Luteolin 7-O-β-glucoside/Luteolin 7-β-D-glucopyranoside/PETUNIDIN/Luteolin-7-O-Beta-D-glucoside/luteolin 7-O-beta-D-glucoside/Luteolin 7-O-β-glucopyranoside/Nephrocizin/Nephrocizine/7-Glucoluteolin/2-(3,4-Dihydroxyphenyl)-5-hydroxy-7-{[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl]oxy}-4H-chromen-4-on/Luteolin-7-O-β-D-glucoside/Galuteolin/Luteoloside/2-(3,4-Dihydroxyphenyl)-5-hydroxy-7-{[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl]oxy}-4H-chromen-4-one/Luteolin 7-β-D-glucoside/4H-1-Benzopyran-4-one, 2-(3,4-dihydroxyphenyl)-7-(β-D-glucopyranosyloxy)-5-hydroxy-/2-(3,4-Dihydroxyphenyl)-5-hydroxy-7-{[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl]oxy}-4H-chromen-4-one/7-Glucosylluteolin/Luteolin 7-O-glucopyranoside/Flavopurposide/Luteolin 7-b-D-Glucopyranoside/Luteolin 7-O-β-D-glucopyranoside/Luteolin 7-O-β-D-glucoside/2-(3,4-Dihydroxyphenyl)-5-hydroxy-4-oxo-4H-chromen-7-yl-β-D-glucopyranoside/Luteolin 7-β-glucoside/Luteolin-7-o-glucoside/Luteolin 7-b-glucoside/2-(3,4-Dihydroxyphenyl)-5-hydroxy-4-oxo-4H-chromen-7-yl β-D-glucopyranoside/Luteolin 7-O-D-glucoside/Cynaroside/glucoluteolin/Luteolin 7-glucoside/2-(3,4-Dihydroxyphenyl)-7-(b-D-glucopyranosyloxy)-5-hydroxy-4H-1-benzopyran-4-one/cinaroside

IUPAC Name

2-(3,4-dihydroxyphenyl)-5-hydroxy-7-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxychromen-4-one

Density

1.7±0.1 g/cm3

Solubility

Methanol; Ethanol; DMF

Flash Point

296.8±27.8 °C

Boiling Point

838.1±65.0 °C at 760 mmHg

Melting Point

InChl

InChl Key

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#:5373-11-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

29024631

Abstract

Autophagy has attracted a great deal of interest in tumour therapy research in recent years. However, the anticancer effect of luteoloside, a naturally occurring flavonoid isolated from the medicinal plant Gentiana macrophylla, on autophagy remains poorly understood in human lung cells. In the present study, we have investigated the anticancer effects of luteoloside on non-small cell lung cancer (NSCLC) cells and demonstrated that luteoloside effectively inhibited cancer cell proliferation, inducing G0/G1 phase arrest associated with reduced expression of CyclinE, CyclinD1 and CDK4; we further found that treatment with luteoloside did not strongly result in apoptotic cell death in NSCLC (A549 and H292) cells. Interestingly, luteoloside induced autophagy in lung cancer cells, which was correlated with the formation of autophagic vacuoles, breakdown of p62, and the overexpression of Beclin-1 and LC3-II, but not in a human bronchial epithelial cell line (BEAS-2B). Notably, pretreatment of cancer cells with 3-MA, an autophagy inhibitor, protected against autophagy and promoted cell viability but not apoptosis. To further clarify whether luteoloside-induced autophagy depended on the PI3K/AKT/mTOR/p70S6K signalling pathway, a major autophagy-suppressive cascade, cells were treated with a combination of AKT inhibitor (LY294002) and mTOR inhibitor (Rap). These results demonstrated that luteoloside induced autophagy in lung cancer cell lines by inhibiting the pathway at p-Akt (Ser473), p-mTOR and p-p70S6K (Thr389). Moreover, we observed that luteoloside-induced cell autophagy was correlated with production of reactive oxygen species (ROS). NAC-mediated protection against ROS clearly implicated ROS in the activation of autophagy and cell death. In addition, the results showed that ROS served as an upstream effector of the PI3K/AKT/mTOR/p70S6K pathway. Taken together, the present study provides new insights into the molecular mechanisms underlying luteoloside-mediated cell death in NSCLC cells and supports luteoloside as a potential anti-cancer agent for targeting NSCLC through the induction of autophagy, inhibition of proliferation and PI3K/AKT/mTOR/p70S6K signalling.

Copyright © 2017. Published by Elsevier Inc.

KEYWORDS

AKT/mTOR/p70S6K signalling; Autophagy; G(0)/G(1) arrest; Luteoloside; NSCLCs; ROS

Title

Luteoloside induces G0/G1 arrest and pro-death autophagy through the ROS-mediated AKT/mTOR/p70S6K signalling pathway in human non-small cell lung cancer cell lines.

Author

Zhou M1, Shen S1, Zhao X1, Gong X2.

Publish date

2017 Dec 9

PMID

29987481

Abstract

Luteoloside is a flavonoid extracted from several natural herbs that exhibits anti-microbial and anti-inflammation properties. Our study mainly identified the anti-inflammatory mechanism of action of luteoloside in Staphylococcus aureus-induced endometritis. Histopathological observations and myeloperoxidase (MPO) activity showed that luteoloside could protect the uterus from S. aureus-induced damage and ameliorate the infiltration of inflammatory cells. Quantitative PCR (qPCR) and ELISA analysis also revealed that luteoloside could decrease the expression of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 and increase the expression of the anti-inflammatory cytokine IL-10 both in vivo and in vitro. However, western blot analysis revealed that luteoloside inhibited the expression of TLR2 and IL-8 and inhibited the phosphorylation of IκBα and NF-κB p65. Moreover, luteoloside inhibited the apoptosis of endometrial epithelial cells (EECs), suppressed the phosphorylation of p53, and decreased the expression of caspase-3 induced by S. aureus. Furthermore, this study showed that luteoloside inhibited the expression of Bax but increased the expression of Bcl-2. These results indicate that luteoloside has anti-inflammatory properties by inhibiting the TLR2 and NF-κB signaling pathways and plays an anti-apoptotic role in S. aureus-induced endometritis, which may be valuable for the clinical treatment of S. aureus-induced inflammation.

KEYWORDS

Bax; Bcl-2; NF-κB; Toll-like receptor 2; caspase-3; endometritis; luteoloside; p-p53

Title

Luteoloside Protects the Uterus from Staphylococcus aureus-Induced Inflammation, Apoptosis, and Injury.

Author

Wang X1,2, Yuan T2, Yin N1, Ma X1, Zhang Z1, Zhu Z1, Shaukat A1, Deng G3.

Publish date

2018 Oct

PMID

30502652

Abstract

Luteoloside, a flavonoid compound, has been reported to have anti-inflammatory, anti-oxidative, antibacterial, antiviral, anticancer, and cardioprotective effects, among others, but its neuroprotective effects have rarely been studied. The purpose of this study was to investigate the protective effect of luteoloside on cerebral ischemia and explore its potential mechanism. Middle cerebral artery occlusion (MCAO) was performed to investigate the effects of luteoloside on cerebral ischemia-reperfusion (I/R). Male Sprague-Dawley rats were randomly divided into six groups: sham, MCAO, luteoloside (20 mg/kg, 40 mg/kg, 80 mg/kg) and nimodipine (4 mg/kg). The results showed that luteoloside alleviated neurologic deficits and cerebral edema as well as improved cerebral infarction and histopathological changes in MCAO rats. Luteoloside significantly inhibited I/R-induced neuroinflammation, as demonstrated by reduced levels of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in the brain tissues of MCAO rats. Furthermore, our results demonstrated that luteoloside significantly suppressed the activation of nuclear factor-kappa B (NF-κB) signaling, upregulated the protein expression of peroxisome proliferator activated receptor gamma (PPARγ) and increased NF-E2-related factor (Nrf2) nuclear accumulation in MCAO rats. Collectively, our findings suggested that luteoloside played a crucial neuroprotective role by inhibiting NF-κB signaling in focal cerebral ischemia in rats. Furthermore, PPARγ and Nrf2 were also important for the anti-inflammatory effect of luteoloside. In addition, our data suggested that luteoloside might be an effective treatment for cerebral ischemia and other neurological disorders.

Copyright © 2018 Elsevier B.V. All rights reserved.

KEYWORDS

Cerebral ischemia; Luteoloside; NF-κB signaling; Neuroinflammation; Nrf2; PPARγ

Title

Luteoloside attenuates neuroinflammation in focal cerebral ischemia in rats via regulation of the PPARγ/Nrf2/NF-κB signaling pathway.

Author

Li Q1, Tian Z1, Wang M1, Kou J1, Wang C1, Rong X1, Li J1, Xie X2, Pang X3.

Publish date

2019 Jan


Description :

Cynaroside is a flavone, a flavonoid-like chemical compound. It is a 7-O-glucoside of luteolin.