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Liguiritigenin-7-O-D-apiosyl-4’-O-D-glucoside

$1,008

  • Brand : BIOFRON

  • Catalogue Number : BN-O2123

  • Specification : 98%(HPLC)

  • CAS number : 199796-12-8

  • Formula : C26H30O13

  • Molecular Weight : 550.52

  • PUBCHEM ID : 124578359

  • Volume : 20mg

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Catalogue Number

BN-O2123

Analysis Method

HPLC,NMR,MS

Specification

98%(HPLC)

Storage

-20℃

Molecular Weight

550.52

Appearance

Powder

Botanical Source

This product is isolated and purified from the roots of Glycyrrhiza uralensis Fisch

Structure Type

Category

SMILES

C1C(OC2=C(C1=O)C=CC(=C2)OC3C(C(CO3)(CO)O)O)C4=CC=C(C=C4)OC5C(C(C(C(O5)CO)O)O)O

Synonyms

Liquiritin apioside/4-[(2S)-7-{[(2S,3R,4R)-3,4-Dihydroxy-4-(hydroxymethyl)tetrahydro-2-furanyl]oxy}-4-oxo-3,4-dihydro-2H-chromen-2-yl]phenyl β-D-glucopyranoside/4H-1-Benzopyran-4-one, 2-[4-(β-D-glucopyranosyloxy)phenyl]-2,3-dihydro-7-[[(2S,3R,4R)-tetrahydro-3,4-dihydroxy-4-(hydroxymethyl)-2-furanyl]oxy]-, (2S)-/Liguiritigenin-7-O-D-apiosyl-4'-O-D-glucoside

IUPAC Name

Applications

Density

1.6±0.1 g/cm3

Solubility

Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.

Flash Point

299.2±27.8 °C

Boiling Point

889.4±65.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C17H18N2O2/c20-16-8-3-1-6-14(16)12-18-10-5-11-19-13-15-7-2-4-9-17(15)21/h1-4,6-9,12-13,20-21H,5,10-11H2

InChl Key

KEABDZDFSMGRQX-DWMQJYMWSA-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#:199796-12-8) 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

11511570

Abstract

A SCHMASSMANN

Gastrointestinal Unit, University of Berne
Inselspital, Berne, Switzerland

B M PESKAR

Department of Experimental Clinical Medicine
Ruhr-University, Bochum, Germany

Cyclooxygenase (COX), the key enzyme for synthesis of prostaglandins, exists in two isoforms (COX-1 and COX-2). COX-1 is constitutively expressed in the gastrointestinal tract in large quantities and has been suggested to maintain mucosal integrity through continuous generation of prostaglandins. COX-2 is induced predominantly during inflammation. On this premise selective COX-2 inhibitors not affecting COX-1 in the gastrointestinal tract mucosa have been developed as gastrointestinal sparing anti-inflammatory drugs. They appear to be well tolerated by experimental animals and humans following acute and chronic (three or more months) administration. However, there is increasing evidence that COX-2 has a greater physiological role than merely mediating pain and inflammation. Thus gastric and intestinal lesions do not develop when COX-1 is inhibited but only when the activity of both COX-1 and COX-2 is suppressed. Selective COX-2 inhibitors delay the healing of experimental gastric ulcers to the same extent as non-COX-2 specific non-steroidal anti-inflammatory drugs (NSAIDs). Moreover, when given chronically to experimental animals, they can activate experimental colitis and cause intestinal perforation. The direct involvement of COX-2 in ulcer healing has been supported by observations that expression of COX-2 mRNA and protein is upregulated at the ulcer margin in a temporal and spatial relation to enhanced epithelial cell proliferation and increased expression of growth factors. Moreover, there is increasing evidence that upregulation of COX-2 mRNA and protein occurs during exposure of the gastric mucosa to noxious agents or to ischaemia-reperfusion. These observations support the concept that COX-2 represents (in addition to COX-1) a further line of defence for the gastrointestinal mucosa necessary for maintenance of mucosal integrity and ulcer healing.

Title

Cyclooxygenase 2—implications on maintenance of gastric mucosal integrity and ulcer healing: controversial issues and perspectives

Author

F HALTER, A TARNAWSKI, A SCHMASSMANN, and B PESKAR

Publish date

2001 Sep

PMID

18513705

Abstract

During aging, changes in the structure of the cerebral cortex of the rat have been seen, but potential changes in neuron number remain largely unexplored. In the present study, stereological methods were used to examine neuron number in the medial prefrontal cortex and primary visual cortex of young adult (85-90 days of age) and aged (19-22 months old) male and female rats in order to investigate any age-related losses. Possible sex differences in aging were also examined since sexually dimorphic patterns of aging have been seen in other measures. An age-related loss of neurons (18-20%), which was mirrored in volume losses, was found to occur in the primary visual cortex in both sexes in all layers except IV. Males, but not females, also lost neurons (15 %) from layer V/VI of the ventral medial prefrontal cortex and showed an overall decrease in volume of this region. In contrast, dorsal medial prefrontal cortex showed no age-related changes. The effects of aging clearly differ among regions of the rat brain and to some degree, between the sexes.

Section 2: Nervous system development, regeneration, aging

KEYWORDS

sex differences, stereology, neuron number, volume, aging, anterior cingulate

Title

Regional variability in age-related loss of neurons from the primary visual cortex and medial prefrontal cortex of male and female rats

Author

M.A. Yates,1 J.A. Markham,1 S.E. Anderson,1 J.R. Morris,1 and J.M. Juraska1,2,*

Publish date

2009 Jul 7.

PMID

31413306

Abstract

Pathway analysis allows us to gain insights into a comprehensive understanding of the molecular mechanisms underlying cancers. Currently, high-throughput multi-omics data and various types of large-scale biological networks enable us to identify cancer-related pathways by comprehensively analyzing these data. Combining information from multidimensional data, pathway databases and interaction networks is a promising strategy to identify cancer-related pathways. Here we present a novel network-based approach for integrative analysis of DNA methylation and gene expression data to extend original pathways. The results show that the extension of original pathways can provide a basis for discovering new components of the original pathway and understanding the crosstalk between pathways in a large-scale biological network. By inputting the gene lists of the extended pathways into the classical gene set analysis (ORA and FCS), we effectively identified the altered pathways which are correlated well with the corresponding cancer. The method is evaluated on three datasets retrieved from TCGA (BRCA, LUAD and COAD). The results show that the integration of DNA methylation and gene expression data through a network of known gene interactions is effective in identifying altered pathways.

Subject terms: Cancer, Genetics

Title

A network-based pathway-extending approach using DNA methylation and gene expression data to identify altered pathways

Author

Jie Li,1 Qiaosheng Zhang,corresponding author1,2 Zhuo Chen,1 Dechen Xu,1 and Yadong Wang1

Publish date

2019