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Esculin

$43

  • Brand : BIOFRON

  • Catalogue Number : BF-E1011

  • Specification : 98%

  • CAS number : 531-75-9

  • Formula : C15H16O9

  • Molecular Weight : 340.28

  • PUBCHEM ID : 5281417

  • Volume : 20mg

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Catalogue Number

BF-E1011

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

340.28

Appearance

White crystalline powder

Botanical Source

Fraxinus chinensis,Bidens pilosa,Bombax ceiba,Actinidia chinensis,Cardamine leucantha

Structure Type

Phenylpropanoids

Category

Standards;Natural Pytochemical;API

SMILES

C1=CC(=O)OC2=CC(=C(C=C21)OC3C(C(C(C(O3)CO)O)O)O)O

Synonyms

Crataegin/7-Hydroxy-2-oxo-2H-chromen-6-yl β-D-glucopyranoside/Enallachrome/vitaminc2/Esculetin 6-β-D-glucoside/POLYDROM/Bicolorin/Esculetin 6-O-glucoside/Polychrom/7-Hydroxy-2-oxo-2H-chromen-6-yl-β-D-glucopyranoside/BICOLOIN/7-Hydroxycoumarin-6-yl β-D-Glucopyranoside Sesquihydrate/Esculin/7-Hydroxy-6-{[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl]oxy}-2H-chromen-2-one/Polychrome/6-(β-D-Glucopyranosyloxy)-7-hydroxy-2H-1-benzopyran-2-one/Esculetin 6-b-D-glucoside/2H-1-Benzopyran-2-one, 6-(β-D-glucopyranosyloxy)-7-hydroxy-/7-Hydroxy-2-oxo-2H-chromen-6-yl β-D-glucopyranoside hydrate (1:1)/Aesculin/Esculetin-6-O-glucoside/2H-1-Benzopyran-2-one, 6-(β-D-glucopyranosyloxy)-7-hydroxy-, hydrate (1:1)/Escosyl

IUPAC Name

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

Density

1.7±0.1 g/cm3

Solubility

Methanol; Ethanol

Flash Point

262.8±25.0 °C

Boiling Point

697.7±55.0 °C at 760 mmHg

Melting Point

203 °C

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#:531-75-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

31202807

Abstract

Aesculin, a natural product from the traditional and widely-used Chinese medicine named Cortex fraxini, has attracted attention as a novel therapeutic modulator of inflammation. However, little is known about its effect on ulcerative colitis (UC). This study aimed to investigate the protective effects and mechanisms of aesculin on colitis. The results showed that, few cytotoxicity of aesculin were shown in vivo and in the RAW264.7 macrophages, while aesculin significantly relieved the symptoms of DSS-induced colitis and restrained the expression of inflammatory factors including iNOS, IL-1β, TNF-α in both peritoneal macrophages and colonic tissues from DSS-induced mice and RAW264.7 macrophages. Of note, aesculin attenuated the activity of NF-κB signaling while promoted the nuclear localization of PPAR-γ in both rectal tissues from DSS-induced mice and LPS-stimulated macrophages. These findings demonstrated that the protection of aesculin against ulcerative colitis might be due to its regulation on the PPAR-γ and NF-κB pathway. Thus, aesculin could serve as a potential therapeutic agent for the treatment of ulcerative colitis.

Copyright © 2019 Elsevier B.V. All rights reserved.

KEYWORDS

Aesculin; Macrophage; NF-κB; PPAR-γ; Ulcerative colitis

Title

Aesculin protects against DSS-Induced colitis though activating PPARγ and inhibiting NF-кB pathway.

Author

Tian X1, Peng Z2, Luo S3, Zhang S1, Li B1, Zhou C4, Fan H5.

Publish date

2019 Aug 15

PMID

30861618

Abstract

The Keap1-Nrf2-ARE system serves as a premier defence mechanism to curb oxidative stress, which remains as one of the major causes of ageing and pathogenesis in various diseases. Nrf2 is the principal master regulator of the cellular defence system, and its activation remains the prospective therapeutic approach against chronic diseases. One of the recent strategies is to disrupt Keap1-Nrf2 protein-protein interaction (PPI) that alters the docking of Keap1 with Nrf2 by compounds occupying a position in the Keap1 blocking the interface with Nrf2. In this study, we made an attempt to identify the compounds with anticancer, antioxidant and anti-inflammatory properties to disrupt Keap1a/b-Nrf2 PPI through in silico molecular docking in zebrafish. The phylogenetic analysis of Keap1 proteins revealed the existence of orthologous Keap1-Nrf2-ARE system in lower vertebrates that includes zebrafish. The DGR domains of zebrafish Keap1a and Keap1b were modelled with Modeller 9.19 using Keap1 of Mus musculus (PDB ID:5CGJ) as template. Based on the docking calculations, top hit compounds were identified to disrupt both Keap1a and Keap1b interaction with Nrf2 which include quercetin 3,4′-diglucoside, flavin adenine dinucleotide disodium salt hydrate, salvianolic acid A, tunicamycin and esculin. The LC50 of esculin in 3 dpf zebrafish larvae is 5 mmol/L, and the qRT-PCR results showed that esculin significantly increased the transcription of Nrf2 target genes-Gstpi, Nqo1, Hmox1a and Prdx1 in 3 dpf zebrafish larvae. These potential hits could serve as safer Nrf2 activators due to their non-covalent disruption of Keap1-Nrf2 PPI and be developed into efficacious preventive/therapeutic agents for various diseases.

© 2019 Nordic Association for the Publication of BCPT (former Nordic Pharmacological Society).

KEYWORDS

Keap1-Nrf2-ARE pathway; esculin; non-covalent interaction; oxidative stress; protein-protein interaction; zebrafish

Title

Identification of compounds that inhibit the binding of Keap1a/Keap1b Kelch DGR domain with Nrf2 ETGE/DLG motifs in zebrafish.

Author

Raghunath A1, Nagarajan R2, Sundarraj K1, Palanisamy K1, Perumal E1.

Publish date

2019 Sep

PMID

30733181

Abstract

Glucocorticoids are widely prescribed for lots of pathological conditions, however, can produce ‘Cushingoid’ side effects including central obesity, glucose intolerance, insulin resistance and so forth. Our study is intended to investigate the improving effects of coumarins on diabetogenic action of dexamethasone in vivo and in vitro and elucidate potential mechanisms. ICR mice treated with dexamethasone for 21 days exhibited decreased body weight, increased blood glucose and impaired glucose tolerance, which were prevented by fraxetin (40 mg/kg/day), esculin (40 mg/kg/day) and osthole (20 mg/kg/day), respectively. Esculin, fraxetin and osthole also could promote glucose uptake in normal C2C12 myotubes, and improve insulin resistance in myotubes induced by dexamethasone. Western blotting results indicated that esculin, fraxetin and osthole could boost Akt activation, stimulate GLUT4 translocation, thus alleviate insulin resistance. Esculin and osthole also could activate AMPK, thereby phosphorylate TBC1D1 at Ser237, and consequently ameliorate diabetogenic action of dexamethasone. Our study indicates coumarins as potential anti-diabetic candidates or leading compounds for drug development.

Copyright © 2019 The Authors. Production and hosting by Elsevier B.V. All rights reserved.

KEYWORDS

Coumarin; Dexamethasone; Esculin; Fraxetin; Insulin resistance; Osthole

Title

Coumarins ameliorate diabetogenic action of dexamethasone via Akt activation and AMPK signaling in skeletal muscle.

Author

Mo Z1, Li L2, Yu H2, Wu Y2, Li H3.

Publish date

2019 Mar


Description :

Esculin Inhibits the Inflammation of LPS-Induced Acute Lung Injury in Mice Via Regulation of TLR/NF-κB Pathways PUMID/DOI:25676436 Inflammation. 2015 Feb 13. In this study, we investigated anti-inflammatory effects of Esculin (ESC) on lipopolysaccharide (LPS)-induced acute lung injury (ALI). ALI was induced in mice by intratracheal instillation of LPS, and Esculin (20 and 40 mg/kg) was given orally 1 h prior to LPS administration. After 6 h, bronchoalveolar lavage fluid (BALF) and lung tissue were collected. Esculin pretreatment decreased LPS-induced evident lung histopathological changes, lung wet-to-dry weight ratio, and lung myeloperoxidase activity. In addition, pretreatment with Esculin inhibited inflammatory cells and proinflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-1β, and interleukin-6 in BALF. Furthermore, we demonstrated that Esculin inhibited the Toll-like receptor-2 (TLR2), Toll-like receptor-4 (TLR4), myeloid differentiation primary response gene-88 (MyD88), and nuclear factor-κB (NF-κB) p65 in LPS-induced ALI. The results indicated that the Esculin had a protective effect on LPS-induced ALI in mice. Protective effect of esculin against prooxidant aflatoxin B1-induced nephrotoxicity in mice. PUMID/DOI:24326591 Mycotoxin Res. 2014 Feb;30(1):25-32. The protective effect of Esculin was further proved by histopathological findings as it exhibited regenerative activities in mice renal tubules against AFB1-induced nephrotoxicity. The results obtained clearly demonstrate that the protective efficacy of Esculin against pro-oxidant AFB1-induced nephrotoxicity in mice might be due to its antioxidants and free radical scavenging properties. Effects of esculin and esculetin on the survival of Escherichia coli O157 in human faecal slurries, continuous-flow simulations of the rumen and colon and in calves. PUMID/DOI:15137927 Br J Nutr. 2004 May;91(5):749-55. The human pathogen Escherichia coli O157:H7 is thought to be spread by direct or indirect contact with infected animal or human faeces. The present study investigated the effects of the plant coumarin Esculin and its aglycone esculetin on the survival of a strain of E. coli O157 under gut conditions. The addition of these compounds to human faecal slurries and in vitro continuous-flow fermenter models simulating conditions in the human colon and rumen caused marked decreases in the survival of an introduced strain of E. coli O157. When four calves were experimentally infected with E. coli O157 and fed Esculin, the pathogen was detected in five of twenty-eight (18 %) of faecal samples examined post-inoculation, compared with thirteen of thirty-five (37 %) of faecal samples examined from five control calves not fed Esculin. Coumarin compounds that occur naturally in dietary plants or when supplemented in the diet probably inhibit the survival of E. coli O157 in the gut. Anti-apoptotic effect of esculin on dopamine-induced cytotoxicity in the human neuroblastoma SH-SY5Y cell line. PUMID/DOI:17904593 Neuropharmacology. 2007 Nov;53(6):724-32 Dopamine (DA), as a neurotoxin, can elicit severe Parkinson's disease-like syndrome by elevating intracellular reactive oxygen species (ROS) levels and apoptotic activity. In this study, we examined the effect of Esculin, which was extracted from Fraxinus sielboldiana blume, on DA-induced cytotoxicity and the underlying mechanism in human neuroblastoma SH-SY5Y cells. Our results suggest that the protective effects of Esculin (10(-7), 10(-6) and 10(-5) M) on DA-induced cytotoxicity may be ascribed to its anti-oxidative properties by reducing ROS level, and its anti-apoptotic effect via protecting mitochondrion membrane potential (DeltaPsim), enhancing superoxide dismutaese (SOD) activity and reduced glutathione (GSH) levels, and regulating P53, Bax and Bcl-2 expression. In addition, Esculin inhibited the release of cytochrome c and apoptosis-inducing factor (AIF), and the protein expression of activated caspase 3. These data indicate that Esculin may provide a useful therapeutic strategy for the treatment of progressive neurodegenerative diseases such as Parkinson's disease (PD). Inhibitory effect of natural coumarin compounds, esculetin and esculin, on oxidative DNA damage and formation of aberrant crypt foci and tumors induced by 1,2-dimethylhydrazine in rat colons. PUMID/DOI:17978474 Biol Pharm Bull. 2007 Nov;30(11):2052-7. The effects of esculetin (6,7-dihydroxycoumarin) and its 6-glycoside, esculin, on 8-oxo-2'-deoxyguanosine (8-oxodG) formation and carcinogenesis induced by a chemical carcinogen, 1,2-dimethylhydrazine (DMH), were examined in the colons of male Fischer 344 rats. Animals were given water containing esculetin or esculin for 7 d before subcutaneous injection of DMH (20 mg/kg body wt), killed 24 h after DMH treatment, and the levels of thiobarbituric acid reactive substances (TBARS) and 8-oxodG in the colons were determined. Both esculetin and esculin suppressed significantly the DMH-induced increases in 8-oxodG and TBARS in rat colon mucosa. We further investigated the modifying effect of esculin intake on the development of DMH-induced colonic aberrant crypt foci (ACF). Animals were given DMH once a week for 4 weeks to induce ACF. They then received water containing esculin ad libitum for 5 weeks (initiation phase) or 11 weeks after DMH treatment (post-initiation phase). Animals in the positive control group received tap water throughout the experiment. At the end of the experiment (16 weeks), the ingestion of esculin during the initiation phase significantly reduced the incidence of gross tumors, the number of ACF per rat and the mean number of AC per focus, while the esculin treatment during the post-initiation phase significantly decreased only the number of ACF per rat. These results suggest that esculin intake has an inhibitory effect on DMH-induced oxidative DNA damage and carcinogenesis in rat colons.