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Forsythin

$43

  • Brand : BIOFRON

  • Catalogue Number : BF-F3007

  • Specification : 98%

  • CAS number : 487-41-2

  • Formula : C27H34O11

  • Molecular Weight : 534.55

  • PUBCHEM ID : 24721571

  • Volume : 25mg

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Catalogue Number

BF-F3007

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

534.55

Appearance

White crystalline powder

Botanical Source

Gleditsia sinensis,Forsythia suspensa,Crepis rigescens,Elaeagnus pungens,Osmanthus fordii

Structure Type

Lignanoids

Category

Standards;Natural Pytochemical;API

SMILES

COC1=C(C=C(C=C1)C2C3COC(C3CO2)C4=C(C=C(C=C4)OC5C(C(C(C(O5)CO)O)O)O)OC)OC

Synonyms

β-D-Glucopyranoside, 4-[(1S,3aR,4R,6aR)-4-(3,4-dimethoxyphenyl)tetrahydro-1H,3H-furo[3,4-c]furan-1-yl]-2-methoxyphenyl/Pillyrin/Chionanthin/4-[(1S,3aR,4R,6aR)-4-(3,4-Dimethoxyphenyl)tetrahydro-1H,3H-furo[3,4-c]furan-1-yl]-2-methoxyphenyl β-D-glucopyranoside/PHILLYRIN/Phillyroside/phyllyrin/[1S-(1a,3aa,4b,6aa)]-4-[4-(3,4-Dimethoxyphenyl)tetrahydro-1H,3H-furo[3,4-c]furan-1-yl]-2-methoxyphenyl-b-D-glucopyranoside

IUPAC Name

(2S,3R,4S,5S,6R)-2-[4-[(3R,3aR,6S,6aR)-3-(3,4-dimethoxyphenyl)-1,3,3a,4,6,6a-hexahydrofuro[3,4-c]furan-6-yl]-3-methoxyphenoxy]-6-(hydroxymethyl)oxane-3,4,5-triol

Applications

Phillyrin is isolated from Forsythia suspensa Vahl (Oleaceae), has antibacterial and anti-inflammatory activities. Phillyrin has potential inductive effects on rat CYP1A2 and CYP2D1 activities, without affecting CYP2C11 and CYP3A1/2 activities[1].

Density

1.4±0.1 g/cm3

Solubility

Methanol

Flash Point

395.5±32.9 °C

Boiling Point

730.4±60.0 °C at 760 mmHg

Melting Point

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2932900000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:487-41-2) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

31832909

Abstract

Damage to the integrity of heparin sulfate (HS) in the endothelial glycocalyx is an important factor of glomerular filtration barrier dysfunction, which is the basic pathological feature of acute kidney injury (AKI). AKI is a common clinical critical illness with few drugs options offering effective treatment. Phillyrin (Phil), the main pharmacological component of Forsythia suspensa, possesses a wide range of pharmacological activities. However, the effects of Phil on lipopolysaccharide (LPS)-induced AKI have yet to be reported. The aim of the present study is to analyze the effects of Phil on HS damage and inflammatory signaling pathways in LPS-induced AKI. Results revealed that Phil reduces pathological changes and improves renal function in LPS-induced AKI. Further analysis indicated that Phil effectively protects against glycocalyx HS degradation in LPS-stimulated EA.hy926 cells in vitro and LPS-induced AKI mice in vivo. The protective effect of Phil on HS damage may be associated with the isolate’s ability to suppress the production of reactive oxygen species, and decrease expression levels of cathepsin L and heparanase in vitro and in vivo. In addition, ELISA and Western blot results revealed that Phil inhibits the activation of the NF-κB and MAPK signaling pathways and decreases the levels of inflammatory cytokines (IL-1β, IL-6, and TNF-α) in LPS-induced ARDS mice. In general, protection against endothelial glycocalyx HS damage and inhibition of inflammatory responses by Phil may be used as treatment targets for LPS-induced AKI.

KEYWORDS

acute kidney injury; heparin sulfate; inflammatory signaling pathways; phillyrin

Title

Phillyrin Relieves Lipopolysaccharide-Induced AKI by Protecting Against Glycocalyx Damage and Inhibiting Inflammatory Responses.

Author

Zhang D1, Qi B1, Li D1, Feng J1, Huang X1, Ma X1, Huang L2, Wang X3, Liu X4.

Publish date

2019 Dec 12

PMID

PMC6811733

Abstract

As the sole cell type responsible for bone resorption, osteoclasts play a pivotal role in a variety of lytic bone diseases. Suppression of osteoclast formation and activation has been proposed as an effective protective therapy for new bone. In this study, we reported for the first time that phillyrin (Phil), an active ingredient extracted from forsythia, significantly inhibited RANKL-induced osteoclastogenesis and bone resorption in vitro and protected against lipopolysaccharide-induced osteolysis in vivo. Further molecular investigations demonstrated that Phil effectively blocked RANKL-induced activations of c-Jun N-terminal kinase and extracellular signal-regulated kinase, which suppressed the expression of c-Fos and nuclear factor of activated T-cells cytoplasmic 1. Taken together, these data suggested that Phil might be a potential antiosteoclastogenesis agent for treating osteoclast-related bone lytic diseases.
Copyright © 2019 Wang, Chen, Zhang, Zhao, Yu, Ma and Liu.

KEYWORDS

MAPK signaling pathway; bone resorption; osteoclast formation; osteolysis; phillyrin

Title

Phillyrin Attenuates Osteoclast Formation and Function and Prevents LPS-Induced Osteolysis in Mice.

Author

Wang J1, Chen G1, Zhang Q1, Zhao F1, Yu X1, Ma X1, Liu M1.

Publish date

2019 Oct 17

PMID

31923823

Abstract

The neuroinflammatory response induced by microglia plays a vital role in causing secondary brain damage after traumatic brain injury (TBI). Previous studies have found that the improved regulation of activated microglia could reduce neurological damage post-TBI. Phillyrin (Phi) is one of the main active ingredients extracted from the fruits of the medicinal plant Forsythia suspensa (Thunb.) with anti-inflammatory effects. Our study attempted to investigate the effects of phillyrin on microglial activation and neuron damage after TBI. The TBI model was applied to induce brain injury in mice, and neurological scores, brain water content, hematoxylin and eosin staining and Nissl staining were employed to determine the neuroprotective effects of phillyrin. Immunofluorescent staining and western blot analysis were used to detect nuclear factor-kappa B (NF-κB) and peroxisome proliferator-activated receptor gamma (PPARγ) expression and nuclear translocation, and the inflammation-related proteins and mRNAs were assessed by western blot analysis and quantitative real-time PCR. The results revealed that phillyrin not only inhibited the proinflammatory response induced by activated microglia but also attenuated neurological impairment and brain edema in vivo in a mouse TBI model. Additionally, phillyrin suppressed the phosphorylation of NF-κB in microglia after TBI insult. These effects of phillyrin were mostly abolished by the antagonist of PPARγ. Our results reveal that phillyrin could prominently inhibit the inflammation of microglia via the PPARγ signaling pathway, thus leading to potential neuroprotective treatment after traumatic brain injury.
Copyright © 2019 Elsevier B.V. All rights reserved.

KEYWORDS

Inflammation; Microglia; PPARγ; Phillyrin; Traumatic brain injury

Title

Phillyrin protects mice from traumatic brain injury by inhibiting the inflammation of microglia via PPARγ signaling pathway.

Author

Jiang Q1, Chen J1, Long X1, Yao X2, Zou X3, Yang Y1, Huang G4, Zhang H5.

Publish date

2020 Feb