Catalogue Number
BF-F2003
Analysis Method
HPLC,NMR,MS
Specification
98%
Storage
2-8°C
Molecular Weight
370.31
Appearance
Off-White crystalline powder
Botanical Source
Xanthoceras sorbifolium,Fraxinus chinensis,Chrozophora sabulosa,Eurycorymbus cavaleriei,Fraxinus sieboldiana
Structure Type
Phenylpropanoids
Category
Standards;Natural Pytochemical;API
SMILES
COC1=C(C(=C2C(=C1)C=CC(=O)O2)OC3C(C(C(C(O3)CO)O)O)O)O
Synonyms
7,8-Dihydroxy-6-methoxycoumarin-8-b-D-glucoside/7-Hydroxy-6-methoxy-2-oxo-2H-chromen-8-yl β-D-glucopyranoside/8-(Glucosyloxy)-6-methoxyumbelliferone/2H-1-Benzopyran-2-one, 8-(β-D-glucopyranosyloxy)-7-hydroxy-6-methoxy-/7-Hydroxy-6-methoxy-8-{[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl]oxy}-2H-chromen-2-one/7-Hydroxy-6-methoxy-8-{[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl]oxy}-2H-chromen-2-on/8-(β-D-Glucopyranosyloxy)-7-hydroxy-6-methoxy-2H-1-benzopyran-2-one/Fraxin/8-(b-D-Glucopyranosyloxy)-7-hydroxy-6-methoxy-2H-1-benzopyran-2-one/Fraxoside/Fraxetin-8-O-glucoside/Fraxetin-8-glucoside/Paviin/7-Hydroxy-6-methoxy-2-oxo-2H-chromen-8-yl-β-D-glucopyranoside/Fraxetol 8-glucoside/7-Hydroxy-6-methoxy-8-{[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl]oxy}-2H-chromen-2-one
IUPAC Name
7-hydroxy-6-methoxy-8-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxychromen-2-one
Density
1.6±0.1 g/cm3
Solubility
Methanol; Ethanol
Flash Point
267.1±26.4 °C
Boiling Point
722.2±60.0 °C at 760 mmHg
Melting Point
205-208ºC
InChl
InChI=1S/C16H18O10/c1-23-7-4-6-2-3-9(18)25-14(6)15(11(7)20)26-16-13(22)12(21)10(19)8(5-17)24-16/h2-4,8,10,12-13,16-17,19-22H,5H2,1H3/t8-,10-,12-,13-,16+/m1/s1
InChl Key
CRSFLLTWRCYNNX-YJDQBUFVSA-N
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#:524-30-1) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
COA
31884094
AIM:
Kidney ischemia reperfusion (IR) injury is an important health problem resulting in acute kidney failure. The oxidative stress and inflammatory process are the underlying mechanisms of IR injury. It has been purposed in this study to research the possible protective effects of fraxin on kidney injury induced by IR.
MATERIAL AND METHODS:
32 Sprague Dawley male rats were divided into 4 groups. The groups were organized as follows; sham, IR, IR + fraxin 10 mg/kg, and IR + 50 mg/kg fraxin groups. Some oxidant, antioxidant and inflammatory parameters were evaluated in kidney tissues removed at the end of our experimental study.
KEY FINDINGS:
It was detected that the oxidant and proinflammatory markers increased and antioxidant parameters decreased in IR group but the results significantly reversed in treatment groups compared to IR group. And also, 8-OHdG, NF-κB, HAVCR1 immunopositivities were at severe levels and these results attenuated in IR fraxin + 10 mg/kg, and IR + fraxin 50 mg/kg groups.
SIGNIFICANCE:
These presented results have shown that fraxin performed protective effects against kidney injury induced by IR.
Copyright © 2019 Elsevier Inc. All rights reserved.
Fraxin; Inflammation; Ischemia reperfusion; Kidney; Oxidative stress
Preventive effects of fraxin on ischemia/reperfusion-induced acute kidney injury in rats.
Topdagı o1, Tanyeli A2, Akdemir FNE3, Eraslan E4, Guler MC2, comaklı S5.
2020 Feb 1
31273573
Acute respiratory distress syndrome (ARDS) is a severe acute disease that threatens human health, and few drugs that can effectively treat this disease are available. Fraxin, one of the main active ingredients of Cortex Fraxini, a Chinese herbal medicine, has presented various pharmacological and biological activities. However, the effects of fraxin on ARDS have yet to be reported. In the present study, the protective effect of fraxin in lipopolysaccharide (LPS)-induced ARDS in a mouse model was analyzed. Results from the hematoxylin and eosin staining showed that fraxin might alleviate pathological changes in the lung tissues of mice with ARDS. ELISA and Western blot results revealed that fraxin might inhibit the production of inflammatory factors, namely, IL-6, TNF-α, and IL-1β, and the activation of NF-κB and MAPK signaling pathways in the lungs. Thus, the inflammatory responses were reduced. Fraxin might inhibit the increase in reactive oxygen species (ROS) and malondialdehyde (MDA), a product of lipid peroxidation in lung tissues. Fraxin might increase the superoxide dismutase (SOD) activity to avoid oxidative damage. Vascular permeability was also assessed through Evans blue dye tissue extravasation and fluorescein isothiocyanate-labeled albumin (FITC-albumin) leakage. Fraxin might inhibit the increase in pulmonary vascular permeability and relieve pulmonary edema. Fraxin was also related to the inhibition of the increase in matrix metalloproteinase-9, which is a glycocalyx-degrading enzyme, and the relief of damages to the endothelial glycocalyx. Thus, fraxin elicited protective effects on mice with LPS-induced ARDS and might be used as a drug to cure ARDS induced by Gram-negative bacterial infection.
ARDS; fraxin; inflammatory responses; lipopolysaccharide; oxidative damages; pulmonary vascular permeability
Fraxin Alleviates LPS-Induced ARDS by Downregulating Inflammatory Responses and Oxidative Damages and Reducing Pulmonary Vascular Permeability.
Ma X1,2, Liu X3, Feng J1,2, Zhang D1,2, Huang L1, Li D1,2, Yin L4, Li L1, Wang XZ2.
2019 Oct
30530164
Fraxin, the effective component of the Chinese traditional medicine Cortex Fraxini, is reported to have anti-inflammatory effects. This study assessed the anti-inflammatory effect of fraxin on the lipopolysaccharide (LPS)-induced inflammatory response in A549 cells and the protective efficacy on LPS-induced acute lung injury (ALI) in mice. Fraxin reduced LPS-induced TNF-α, IL-6 and IL-1β production in A549 cells and alleviated the LPS-induced wet/dry (W/D) weight ratio and the effects observed via histopathological examination of the lung in vivo. Furthermore, fraxin reduced the protein concentrations in the broncho-alveolar lavage (BAL) fluid and cytokine production in the sera. Fraxin also clearly attenuated the oxidation index, including the activity of myeloperoxidase (MPO), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH). Immunohistochemistry analysis showed that fraxin suppressed LPS-induced inflammatory damage. The expression of proteins involved in the NF-κB and NLRP3 inflammatory corpuscle signalling pathways was consistent between the lung tissues and cell samples. Overall, fraxin played a protective role in LPS-induced lung injury by inhibiting the NF-κB and NLRP3 signalling pathways.
Copyright © 2018 Elsevier B.V. All rights reserved.
Acute lung injury; Fraxin; NF-κB pathway; NLRP3 inflammasome
Fraxin ameliorates lipopolysaccharide-induced acute lung injury in mice by inhibiting the NF-κB and NLRP3 signalling pathways.
Li W1, Li W2, Zang L2, Liu F2, Yao Q2, Zhao J2, Zhi W2, Niu X3.
2019 Feb
