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Forsythoside A

$113

  • Brand : BIOFRON

  • Catalogue Number : BF-F2001

  • Specification : 98%

  • CAS number : 79916-77-1

  • Formula : C29H36O15

  • Molecular Weight : 624.59

  • PUBCHEM ID : 5281773

  • Volume : 20mg

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Catalogue Number

BF-F2001

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

-20℃

Molecular Weight

624.59

Appearance

Off-White crystal

Botanical Source

Houttuynia cordata,Forsythia suspensa

Structure Type

Phenylpropanoids

Category

Standards;Natural Pytochemical;API

SMILES

CC1C(C(C(C(O1)OCC2C(C(C(C(O2)OCCC3=CC(=C(C=C3)O)O)O)O)OC(=O)C=CC4=CC(=C(C=C4)O)O)O)O)O

Synonyms

Forsythiaside/β-D-Glucopyranoside, 2-(3,4-dihydroxyphenyl)ethyl 6-O-(6-deoxy-α-L-mannopyranosyl)-4-O-[(2E)-3-(3,4-dihydroxyphenyl)-1-oxo-2-propen-1-yl]-/2-(3,4-Dihydroxyphenyl)ethyl 6-O-(6-deoxy-α-L-mannopyranosyl)-4-O-[(2E)-3-(3,4-dihydroxyphenyl)prop-2-enoyl]-β-D-glucopyranoside/2-(3,4-Dihydroxyphenyl)ethyl 6-O-(6-deoxy-α-L-mannopyranosyl)-4-O-[(2E)-3-(3,4-dihydroxyphenyl)-2-propenoyl]-β-D-glucopyranoside/forsytoside A/Forsythiaside A/forsythoside

IUPAC Name

[(2R,3S,4R,5R,6R)-6-[2-(3,4-dihydroxyphenyl)ethoxy]-4,5-dihydroxy-2-[[(2R,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxymethyl]oxan-3-yl] (E)-3-(3,4-dihydroxyphenyl)prop-2-enoate

Density

1.6±0.1 g/cm3

Solubility

Methanol; Water

Flash Point

295.7±27.8 °C

Boiling Point

911.9±65.0 °C at 760 mmHg

Melting Point

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2932990000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:79916-77-1) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

31173213

Abstract

Ischemic stroke is a common type of stroke with a high mortality and morbidity rate. Preventing and controlling cerebral ischemic injury is particularly important. Forsythiaside A (FA) has been reported to have anti‑inflammatory and antioxidant activities. The aim of the present study was to explore the impact of FA on middle cerebral artery occlusion (MCAO)‑induced cerebral ischemic injury in rats. The results indicated that FA markedly increased the percent survival and decreased the neurological deficit score in rats with cerebral ischemic injury. Furthermore, cell apoptosis was significantly inhibited by FA administration, which was accompanied by decreased caspase‑3 and caspase‑9 expression. A marked increase in the expression levels of nuclear factor‑erythroid 2‑related factor 2 (Nrf2), NAD(P)H quinone dehydrogenase 1 and glutathione‑s‑transferase was detected in FA‑treated rats. In addition, treatment with FA reduced malonaldehyde expression, and enhanced the expression of superoxide dismutase and glutathione. Furthermore, endoplasmic reticulum (ER) stress was vastly alleviated by FA treatment, as evidenced by the increased expression of B‑cell lymphoma 2, apoptosis regulator and the downregulated expression of phosphorylated (phospho)‑protein kinase RNA‑like ER kinase (PERK)/PERK, phospho‑inositol‑requiring enzyme 1 (IRE1α)/IRE1α and CCAAT‑enhancer‑binding proteins homologous protein. Taken together, the present study demonstrated that FA attenuated cerebral ischemic damage via mediation of the activation of Nrf2 and ER stress pathways. These data may provide ideas for novel treatment strategies of cerebral ischemic damage.

Title

Forsythiaside A protects against focal cerebral ischemic injury by mediating the activation of the Nrf2 and endoplasmic reticulum stress pathways.

Author

Ma T1, Shi YL2, Wang YL3.

Publish date

2019 Aug

PMID

30798212

Abstract

Forsythia suspensa metabolites have many bioactivities, such as selective immuno suppression, antioxidation, anti-hepatic injury, etc. In the present study, the interactions of the three metabolites with BSA have been investigated in a buffer (pH 7.40) using multi-spectroscopic techniques in combination with molecular docking methods. Two isoformers, forsythoside A and forsythoside I can statically quench BSA intrinsic fluorescence by forming the complexes with BSA at stoichiometric ratio of 1:1 that is again proved by UV-visible absorption. During the binding, the proportion of α-helix in BSA increases, the microenvironment around Tryptophan 213 changes and FRET is one of the major factors to quench fluorescence. Forsythoside E forms BSA-forsythoside E complex (1:1) and thus enhances the intrinsic fluorescence of BSA. During the process, forsythoside E affects not only Tryptophan residues but also Tyrosine residues so that the conformation of BSA is consequently changed. All above binding processes are spontaneous mainly through hydrogen bonding and the hydrophobic force interaction, which is supported by docking analysis and thermodynamic parameters. In addition, three compounds do not induce BSA aggregation. These findings are beneficial to understand the detailed information of the interactions of Forsythia suspensa metabolites with BSA.

Copyright © 2019. Published by Elsevier B.V.

KEYWORDS

Bovine serum albumin (BSA); Forsythia suspensa; Interaction; Metabolites; Spectroscopy

Title

Different effects of Forsythia suspensa metabolites on bovine serum albumin (BSA).

Author

Li Y1, Guo Q1, Yan Y1, Chen T1, Du C2, Du H3.

Publish date

2019 May 5;

PMID

30769029

Abstract

In the study, the neuroprotectivities of forsythiaside, a main constituent of Forsythia suspensa (Thunb.) Vahl (F. suspensa, Lianqiao in Chinese), were investigated in the hippocampal slices. Forsythiaside suppressed the overexpression of cyclooxygenase-2 (COX-2) and monoacylglycerol lipase (MAGL) proteins induced by β-amyloid (Aβ25-35) to upregulate the levels of 2-arachidonoylglycerol (2-AG), an endogenous endocannabinoids. Then the inhibition of forsythiaside on COX-2 was deeply studied by the molecular docking. Forsythiaside prevented neuroinflammation and apoptosis from Aβ25-35 insults, and this action appeared to be mediated via cannabinoid receptor 1 (CB1R)-dependent nuclear factor-κB (NF-κB) signaling pathways. More importantly, forsythiaside functionally improved Aβ25-35-induced learning and memory deficits, which was indicated by long term potentiation (LTP). Taken together, forsythiaside may have therapeutic potential for Alzheimer’s diseases (AD) by increasing the levels of 2-AG.

Copyright © 2019. Published by Elsevier Ltd.

KEYWORDS

2-Arachidonoylglycerol; Cyclooxygenase-2; Forsythiaside; Long term potentiation; Neuroinflammation; β-Amyloid

Title

Forsythiaside prevents β-amyloid-induced hippocampal slice injury by upregulating 2-arachidonoylglycerol via cannabinoid receptor 1-dependent NF-κB pathway.

Author

Chen L1, Yan Y1, Chen T1, Zhang L1, Gao X1, Du C2, Du H3.

Publish date

2019 May


Description :

Forsythiaside A, a phenylethanoside product isolated from air-dried fruits of Forsythia suspense, has anti-inflammatory and antioxidant effects[1].