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Catalogue Number
BD-D1311
Analysis Method
HPLC,NMR,MS
Specification
98%(HPLC)
Storage
2-8℃
Molecular Weight
592.55
Appearance
White crystalline powder
Botanical Source
Cirsium setosum (Willd.) MB.
Structure Type
Flavonoids
Category
Standards;Natural Pytochemical;API
SMILES
CC1C(C(C(C(O1)OCC2C(C(C(C(O2)OC3=CC(=C4C(=C3)OC(=CC4=O)C5=CC=C(C=C5)OC)O)O)O)O)O)O)O
Synonyms
Acaciin/4H-1-Benzopyran-4-one, 7-[[6-O-(6-deoxy-α-L-mannopyranosyl)-β-D-glucopyranosyl]oxy]-5-hydroxy-2-(4-methoxyphenyl)-/5-Hydroxy-2-(4-methoxyphenyl)-7-{[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-({[(2R,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyltetrahydro-2H-pyran-2-yl]oxy}methyl)tetrahydro-2H-pyran-2-yl]oxy}-4H-chromen-4-one/Buddleoglucoside/Acacetin 7-rutinoside/5-Hydroxy-2-(4-methoxyphenyl)-4-oxo-4H-chromen-7-yl-6-O-(6-deoxy-α-L-mannopyranosyl)-β-D-glucopyranoside/Acacetin 7-O-rutinoside/Acacetin 7-O-α-L-rhamnopyranosyl-(16)-β-D-glucopyranoside/acacetin-7-O-ramnosyl-glucoside/linarin/Acacetin-7-O-β-D-rutinoside/5,7-Dihydroxy-4'-methoxyflavone-D-glucosido-L-rhamnoside/Acacetin-b-rutinoside/Linarigenin-glucoside/5-Hydroxy-2-(4-methoxyphenyl)-4-oxo-4H-chromen-7-yl 6-O-(6-deoxy-α-L-mannopyranosyl)-β-D-glucopyranoside/Acacetin-7-rutinoside/Buddleoflavonoloside/Linaric acid/7-[[6-O-(6-Deoxy-a-L-mannopyranosyl)-b-D-glucopyranosyl]oxy]-5-hydroxy-2-(4-methoxyphenyl)-4H-benzopyran-4-one/Acacetin-7-O-rutinoside/Buddleoside/apigenin-4'-methylether-7-O-rutinoside
IUPAC Name
5-hydroxy-2-(4-methoxyphenyl)-7-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-[[(2R,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxymethyl]oxan-2-yl]oxychromen-4-one
Applications
Density
1.6±0.1 g/cm3
Solubility
Methanol; DMF; DMSO
Flash Point
292.2±27.8 °C
Boiling Point
885.2±65.0 °C at 760 mmHg
Melting Point
258-260ºC
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#:480-36-4) 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.
30802512
BACKGROUND:
Due to complex pathogenesis of Alzheimer’s disease (AD), currently there is no effective disease-modifying treatment. Acetylcholinesterase (AChE) has introduced itself as an important target for AD therapy. Linarin as the representative active ingredient of flavonoid glycoside in Flos chrysanthemi indici has been found to have anti-acetylcholinesterase effect.
AIMS:
The present study intended to explore the potential effect of linarin for treatment of AD.
MAIN METHODS:
In this study, molecular docking simulation was used to evaluate whether linarin could dock with AChE and decipher the mechanism of linarin as an AChE inhibitor. After molecular docking simulation, AlCl3-induced Alzheimer’s disease zebrafish model was established. Effects of linarin on treating AD zebrafish dyskinesia and AChE inhibition were compared with donepezil (DPZ) which was used as a positive control drug.
KEY FINDINGS:
Molecular docking simulation showed that linarin plays a critical role in AChE inhibition by binding AChE active sites. The experiments illustrated that the dyskinesia recovery rate of AD zebrafish could be significantly improved by linarin. The dyskinesia recovery and AChE inhibition rate were 88.0% and 74.5% respectively, while those of DPZ were 79.3% and 43.6%.
SIGNIFICANCE:
These findings provide evidences for supporting linarin to be developed into an AD drug by inhibiting the activity of AChE.
Copyright © 2019 Elsevier Inc. All rights reserved.
Acetylcholinesterase inhibitor; Alzheimer's disease; Linarin; Zebrafish
Linarin improves the dyskinesia recovery in Alzheimer's disease zebrafish by inhibiting the acetylcholinesterase activity.
Pan H1, Zhang J1, Wang Y1, Cui K1, Cao Y1, Wang L2, Wu Y3.
2019 Apr 1
29845284
Acute lung injury (ALI) is an important cause of morbidity and mortality for critically ill patients, and linarin (LR) may be a potential treatment for ALI as it reportedly has antioxidant, anti‑inflammatory and apoptotic‑regulating activity. In the present study, the authors report that saline and LR (12.5, 25 and 50 mg/kg) were applied to male C57BL/6 mice via gavage. Then, mice were intratracheally injected with either saline or lipopolysaccharide (LPS). LR‑pretreatment attenuated LPS‑induced ALI and platelet activation and reduced CD41 expression levels and neutrophil platelet aggregates. Additionally, LPS‑triggered pulmonary myeloperoxidase activity and neutrophil infiltration in lung tissues, and this was eliminated by LR dose‑dependently. Furthermore, LPS‑induced oxidative stress and pro‑inflammatory cytokine release were downregulated by LR by inhibiting thioredoxin‑interacting protein and nuclear factor‑κB signaling pathways, including their downstream and upstream signals, such as xanthine oxidase, NLR family WHAT, pyrin domain‑containing 3 (NLRP3), apoptosis‑associated speck‑like protein containing a C‑terminal caspase recruitment domain (ASC), caspase‑1, IκB kinase‑α (IKK‑α) and IκBα. Moreover, in LPS‑induced mice, the mitogen‑activated protein kinase pathway was inactivated by LR. In vitro, LR reduced LPS‑induced inflammation and oxidative stress, which was linked to reduction of ROS. In conclusion, LR pretreatment may be protective against LPS‑induced ALI.
Acetylcholinesterase inhibitor; Linarin; Mice brain; Molecular docking study
Linarin prevents LPS‑induced acute lung injury by suppressing oxidative stress and inflammation via inhibition of TXNIP/NLRP3 and NF‑κB pathways.
Han X1, Wu YC1, Meng M1, Sun QS1, Gao SM1, Sun H1.
2018 Sep
28340376
OBJECTIVES:
As we all know, oxidative stress was one of the most important causes of ischemia-reperfusion injury. And it was reported that Nrf-2 as an important regulator for oxidative stress could be activated by Linarin. Thus it would be interesting to find whether Linarin could inhibit ischemia-reperfusion injury through activating Nrf-2.
METHODS:
In this study, cell activity was detected by MTT assay and caspase-3 activity detection kit. And the expressions or activities of some signal proteins were evaluated by western-blot or activity detection kits. At last, the effect and mechanism of Linarin on heart tissues were verified in the ischemia-reperfusion model of isolated hearts.
RESULTS:
The proliferation activity of cell was inhibited while the apoptosis rate was increased after hypoxia-reoxygenation. However, Linarin could inhibit these two variations. It was found that these effects of Linarin were related with the activation of Nrf-2 through PI3K/Akt signaling pathway. Meanwhile, the anti-oxidative enzymes, regulated by Nrf-2, were enhanced to against the oxidative stress caused by hypoxia-reoxygenation. And with the inhibition of oxidative stress, some proliferation and apoptosis related proteins such as NF-kB and Cytochrome C were adjusted to support the viability of cells. At last, these results were verified in the ischemia reperfusion experiment of isolated hearts.
CONCLUSIONS:
From this study, we assured that LIN could protect myocardial tissue from ischemia-reperfusion through activating Nrf-2.
Ischemia-reperfusion injury; Linarin; Myocardial cell; Nrf-2; Oxidative stress
Linarin could protect myocardial tissue from the injury of Ischemia-reperfusion through activating Nrf-2.
Yu Q1, Li X2, Cao X3
2017 Jun
