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Myricitrin

$198

  • Brand : BIOFRON

  • Catalogue Number : BF-M3019

  • Specification : 95%

  • CAS number : 17912-87-7

  • Formula : C21H20O12

  • Molecular Weight : 464.38

  • PUBCHEM ID : 5281673

  • Volume : 1000mg

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Catalogue Number

BF-M3019

Analysis Method

HPLC,NMR,MS

Specification

95%

Storage

2-8°C

Molecular Weight

464.38

Appearance

Yellow crystalline powder

Botanical Source

Myrica rubra,Ailanthus fordii,Ampelopsis grossedentata,Juglans mandshurica,Mangifera indica

Structure Type

Flavonoids

Category

Standards;Natural Pytochemical;API

SMILES

CC1C(C(C(C(O1)OC2=C(OC3=CC(=CC(=C3C2=O)O)O)C4=CC(=C(C(=C4)O)O)O)O)O)O

Synonyms

5,7-Dihydroxy-4-oxo-2-(3,4,5-trihydroxyphenyl)-4H-chromen-3-yl 6-deoxy-α-L-mannopyranoside/4H-1-Benzopyran-4-one, 3-[(6-deoxy-α-L-mannopyranosyl)oxy]-5,7-dihydroxy-2-(3,4,5-trihydroxyphenyl)-/Myricetol 3-rhamnoside/Myricitroside/5,7-Dihydroxy-3-{[(2S,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyltetrahydro-2H-pyran-2-yl]oxy}-2-(3,4,5-trihydroxyphenyl)-4H-chromen-4-one/5,7-Dihydroxy-4-oxo-2-(3,4,5-trihydroxyphenyl)-4H-chromen-3-yl 6-deoxy-a-L-mannopyranoside/EINECS 241-856-7/3,3',4',5,5',7-Hexahydroxyflavone 3-O-Rhamnoside/Myricetrin/5,7-Dihydroxy-3-{[(2S,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyltetrahydro-2H-pyran-2-yl]oxy}-2-(3,4,5-trihydroxyphenyl)-4H-chromen-4-on/Myricetin-3-Rhamnoside/Myricetin 3-O-α-L-rhamnoside/5,7-Dihydroxy-4-oxo-2-(3,4,5-trihydroxyphenyl)-4H-chromen-3-yl-6-deoxy-α-L-mannopyranoside/Myricitrin (8CI)/Myricetin 3-O-α-rhamnopyranoside/Myricetin 3-Rhamnoside/5,7-Dihydroxy-3-{[(2S,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyltetrahydro-2H-pyran-2-yl]oxy}-2-(3,4,5-trihydroxyphenyl)-4H-chromen-4-one/Myricetin 3-O-α-L-rhamnopyranoside/Myricitrine/myricetin-3-O-rhamnoside/3,3',4',5,5',7-Hexahydroxyflavone 3-rhamnoside/Myricitrin/Myricetin 3-O-rhamnoside

IUPAC Name

5,7-dihydroxy-3-[(2S,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxy-2-(3,4,5-trihydroxyphenyl)chromen-4-one

Density

1.9±0.1 g/cm3

Solubility

Methanol; Ethanol; Acetontrile; DMSO

Flash Point

315.7±27.8 °C

Boiling Point

896.6±65.0 °C at 760 mmHg

Melting Point

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#:17912-87-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

29568905

Abstract

It is necessary to identify compounds that may provide protection against alcoholic liver disease. To the best of our knowledge, the effect of myricitrin on the development of ethanol‑induced liver disease has not been previously investigated. The present study aimed to determine the effect of myricitrin on ethanol‑induced steatosis in AML12 mouse liver cells and to identify the underlying molecular mechanisms. Ethanol‑treated AML12 cells exhibited significant improvement in viability following treatment with myricitrin. Oil red O staining indicated that myricitrin ameliorated ethanol‑induced lipid accumulation in cells. Furthermore, following treatment with myricitrin, improvement in ethanol‑induced steatosis and decrease in the levels of reactive oxygen species and lipoperoxides were observed in ethanol‑stimulated cells. Myricitrin suppressed mRNA and protein expression of tumor necrosis factor‑α, interleukin‑6 and transforming growth factor‑β1 in ethanol‑stimulated AML12 cells. Myricitrin markedly increased phosphorylation of adenosine monophosphate‑activated protein kinase (AMPK) and significantly reduced mRNA expression of sterol‑regulatory element‑binding protein‑1c (SREBP‑1c) and fatty acid synthase in ethanol‑stimulated AML12 cells. The results of the present study indicate that myricitrin ameliorates ethanol‑induced steatosis in AML12 cells by attenuating oxidative stress, suppressing expression of certain inflammatory cytokines and modulating the AMPK/SREBP-1c pathway.

Title

Myricitrin Ameliorates Ethanol-Induced Steatosis in Mouse AML12 Liver Cells by Activating AMPK, and Reducing Oxidative Stress and Expression of Inflammatory Cytokines

Author

Jing Gao 1 , Si Chen 1 , Zikai Qiu 2 , Liping Fang 1 , Lishan Zhang 1 , Chang Guo 1 , Tong Chen 1 , Longxin Qiu 1

Publish date

2018 May

PMID

28751937

Abstract

Myricitrin, a naturally occurring polyphenol hydroxy flavonoid, has been reported to possess anti-inflammatory properties. However, the precise molecular mechanism of myricitrin’s effects on LPS-induced inflammation is unclear. In the present study, myricitrin significantly alleviated acute lung injury in mice. Myricitrin also markedly suppressed the production of NO, TNF-α, IL-6, and MCP-1 in RAW264.7 macrophage cells. The inhibition of NO was concomitant with a decrease in the protein and mRNA levels of iNOS. The phosphorylation of JAKs and STAT-1 was abrogated by myricitrin. Furthermore, myricitrin inhibited the nuclear transfer and DNA binding activity of STAT1. The JAK-specific inhibitor ruxolitinib simulated the anti-inflammatory effect of myricitrin. However, myricitrin had no impact on the MAPK signalling pathway. Myricitrin attenuated the generation of intracellular ROS by inhibiting the assembly of components of the gp91phox and p47phox. Suppression of ROS generation using NAC or apocynin or by silencing gp91phox and p47phox all demonstrated that decreasing the level of ROS inhibited the LPS-induced inflammatory response. Collectively, these results confirmed that myricitrin exhibited anti-inflammatory activity by blocking the activation of JAKs and the downstream transcription factor STAT1, which may result from the downregulation of NOX2-dependent ROS production mediated by myricitrin.

Title

Myricitrin Modulates NADPH Oxidase-Dependent ROS Production to Inhibit Endotoxin-Mediated Inflammation by Blocking the JAK/STAT1 and NOX2/p47 phox Pathways

Author

Shimei Qi 1 2 , Zunyong Feng 1 3 , Qiang Li 1 2 , Zhilin Qi 1 2 , Yao Zhang 1 2

Publish date

2017

PMID

31865448

Abstract

The present study investigated the anti-atherosclerotic potential of myricitrin in hypercholesterolemic rats. Rats were divided into the following groups: sham (standard food), control [1% high-cholesterol diet (HCD)], 1 μM myricitrin + 1% HCD, 10 μM myricitrin + 1% HCD, 100 μM myricitrin + 1% HCD, and the positive control (10 mg/kg body weight atorvastatin). The dose was given to rats via oral gavage for 45 consecutive days. Feeding of rats with 1% HCD caused substantial increases in the levels of LDL, cholesterol, and triglycerides (TG), while high-density lipoprotein (HDL) was reduced. However, rats supplemented with myricitrin had reduced levels of cholesterol, LDL, and TG to near-normal levels, whereas HDL was increased. Catalase, superoxide dismutase (SOD), glutathione peroxidase (Gpx), and reduced glutathione (GSH) levels were substantially reduced in the HCD-fed rats compared with sham rats. However, the rats supplemented with 100 μM myricitrin showed > 50% increases in these levels. Lipid peroxidation and reactive oxygen species (ROS) levels were reduced following myricitrin treatment. The aortic cell wall area was significantly increased by 14.5% in HCD-fed rats. However, rats supplemented with 1, 10, and 100 μM myricitrin showed significant reductions in the aortic cell wall area of 2.3%, 4%, and 27.5%, respectively. This is the first report of the anti-atherosclerotic and hypolipidemic effects of myricitrin in hypercholesterolemic rats. Myricitrin decreased the level of total serum cholesterol and the role of aortic atherosclerosis in hypercholesterolemic rats.

KEYWORDS

Anatioxidants; Atherosclerosis; Cholesterol; Myricitrin; Rats.

Title

Myricitrin Exhibits Anti-Atherosclerotic and Anti-Hyperlipidemic Effects in Diet-Induced Hypercholesterolemic Rats

Author

Jing Gao 1 , Cuicui Liu 2 , Heping Zhang 1 , Zhen Sun 1 , Rongmei Wang 3

Publish date

2019 Dec 21


Description :

Phytochemical profile of the aerial parts of Sedum sediforme and anti-inflammatory activity of myricitrin. PUMID/DOI:25920226 Nat Prod Commun. 2015 Jan;10(1):83-8. The aim of this study was to investigate the phytochemical profile of the methanol extract of the aerial parts of Sedum sediforme and to identify its secondary metabolites. By means of chromatographic separation and enrichment of compounds, HPLC-ESI-MS, HRMS, 1D-, 2D- NMR and/or comparison with reference compounds, three triterpenes, two sterols, ten flavonoids and twelve phenolic compounds were identified, together with two new compounds, i.e. (2R*, 3R*)-5,7-dihydroxy-2,3-dimethyl-4-chromanone-7-O-β-D-glucoside (27) and butan-2-O-rutinoside (28). Out of the 29 identified secondary metabolites, 18 are described as ingredients of S. sediforme herein for the first time. Furthermore, Myricitrin, one of the major constituents, was tested for its ability to inhibit different enzymes within the arachidonic acid cascade in order to determine its anti-inflammatory properties. Whereas there was only either weak or no inhibition of the microsomal prostaglandin E2 synthase-1 (mPGES-1) and the soluble epoxide hydrolase (sEH), Myricitrin showed strong inhibition of 5-lipoxygenase (5-LO), with an IC50 of 7.8 ± 0.2 μM. Myricitrin attenuates endothelial cell apoptosis to prevent atherosclerosis: An insight into PI3K/Akt activation and STAT3 signaling pathways. PUMID/DOI:25849952 Vascul Pharmacol. 2015 Apr 4. Blood vessel endothelial dysfunction induced by oxidized low-density lipoprotein (ox-LDL) has been implicated in the pathogenesis of atherosclerosis and vasculopathy. The ox-LDL-elicited reactive oxygen species (ROS) release has been assumed to serve a critical function in endothelial damage. Myricitrin (from Myrica cerifera) is a natural antioxidant that has strong anti-oxidative, anti-inflammatory, and anti-nociceptive activities. However, the protective effect of Myricitrin on ROS-induced endothelial cell injury and its related molecular mechanisms have never been investigated. This study demonstrates that Myricitrin can inhibit ox-LDL-induced endothelial apoptosis and prevent plaque formation at an early stage in an atherosclerotic mouse model. The administration of Myricitrin in vivo decreases the thickness of the vascular wall in the aortic arch of ApoE-/- mice. In vitro study shows that ox-LDL-induced human umbilical vein endothelial cell apoptosis can be reduced upon receiving Myricitrin pre-treatment. Treatment with Myricitrin significantly attenuated ox-LDL-induced endothelial cell apoptosis by inhibiting LOX-1 expression and by increasing the activation of the STAT3 and PI3K/Akt/eNOS signaling pathways. At the same time, our result demonstrates that Myricitrin treatment optimizes the balance of pro/anti-apoptosis proteins, including Bax, Bad, XIAP, cIAP-2, and survivin. Our study suggests that Myricitrin treatment can effectively protect cells from ox-LDL-induced endothelial cell apoptosis, which results in reduced atherosclerotic plaque formation. This result indicates that Myricitrin can be used as a drug candidate for the treatment of cardiovascular diseases. Myricitrin exhibits antioxidant, anti-inflammatory and antifibrotic activity in carbon tetrachloride-intoxicated mice. PUMID/DOI:25656916 Chem Biol Interact. 2015 Mar 25;230:21-9. Myricetin-3-O-α-rhamnoside (Myricitrin) is a naturally occurring phenolic compound which possesses antioxidant and anti-inflammatory activity. The aim of this study was to determine the hepatoprotective effects of Myricitrin. Myricitrin at doses of 10, 30 and 100 mg/kg and silymarin at dose of 100mg/kg were administered to BALB/cN mice by oral gavage, once daily for two consecutive days following carbon tetrachloride (CCl4)-intoxication. Myricitrin significantly ameliorated CCl4-induced increase in serum aspartate transaminase (AST) and alanine transaminase (ALT) levels and histopathological changes in the liver. Hepatic oxidative stress was reduced by Myricitrin, as evidenced by the decrease in lipid peroxidation, with concomitant increase in glutathione (GSH) level and cytochrome P450 2E1 (CYP2E1) expression. In addition, cyclooxygenase-2 (COX-2) and tumor necrosis factor-alpha (TNF-α) overexpression in the liver was reduced, suggesting the suppression of inflammation. The expression of transforming growth factor-beta1 (TGF-β1) and alpha-smooth muscle actin (α-SMA) was markedly ameliorated, indicating the inhibition of profibrotic response. Myricitrin also improved the regeneration of hepatic tissue after CCl4-intoxication, as evidenced by increased proliferating cell nuclear antigen (PCNA) expression. The results of the current study suggest that Myricitrin exhibits a significant hepatoprotective activity. Myricitrin provided better hepatoprotection when compared to silymarin, which is consistent with its higher in vitro antioxidant potential. Analysis of the antinociceptive effect of the flavonoid myricitrin: evidence for a role of the L-arginine-nitric oxide and protein kinase C pathways. PUMID/DOI:16260583 Send to J Pharmacol Exp Ther. 2006 Feb;316(2):789-96. Epub 2005 Oct 31. The present study investigated the antinociceptive effects of the flavonoid Myricitrin in chemical behavioral models of pain in mice and rats. Myricitrin given by i.p. or p.o. routes produced dose-related antinociception when assessed on acetic acid-induced visceral pain in mice. In addition, the i.p. administration of Myricitrin exhibited significant inhibition of the neurogenic pain induced by intraplantar (i.pl.) injection of capsaicin. Like-wise, Myricitrin given by i.p. route reduced the nociception produced by i.pl. injection of glutamate and phorbol myristate acetate (PMA). Western blot analysis revealed that Myricitrin treatment fully prevented the protein kinase C (PKC) alpha and PKCepsilon activation by PMA in mice hind paws. Myricitrin given i.p. also inhibited the mechanical hyperalgesia induced by bradykinin, without affecting similar responses caused by epinephrine and prostaglandin E(2). The antinociception caused by Myricitrin in the acetic acid test was significantly attenuated by i.p. treatment of mice with the nitric oxide precursor, L-arginine. In contrast, Myricitrin antinociception was not affected by naloxone (opioid receptor antagonist) or neonatal pretreatment of mice with capsaicin and Myricitrin antinociceptive effects is not related to muscle relaxant or sedative action. Together, these results indicate that Myricitrin produces pronounced antinociception against chemical and mechanical models of pain in rodents. The mechanisms involved in their actions are not completely understood but seem to involve an interaction with nitric oxide-L-arginine and protein kinase C pathways. Myricitrin, a nitric oxide and protein kinase C inhibitor, exerts antipsychotic-like effects in animal models. PUMID/DOI:21689712 Prog Neuropsychopharmacol Biol Psychiatry. 2011 Aug 15;35(7):1636-44. Myricitrin is a nitric oxide (NO) and protein kinase C (PKC) inhibitor that has central nervous system activity, including anxiolytic-like action. Nitric oxide inhibitors blocked the behavioral effects of apomorphine, suggesting an antipsychotic-like effect. Furthermore, PKC inhibition reduced psychotic symptoms in acute mania patients and blocked amphetamine-induced hyperlocomotion, suggesting a potential antipsychotic-like effect. The present study evaluated the effects of Myricitrin in animal models that assess antipsychotic-like effects (apomorphine-induced stereotypy and climbing and the paw test) and extrapyramidal side effects (catalepsy test and paw test). Olanzapine was used as a positive control. 7-Nitroindazole (7-NI), a NOS inhibitor, and l-arginine, a NO precursor, were used to evaluate nitrergic modulation, and tamoxifen was used to test the effect of PKC inhibition. In mice, Myricitrin dose-dependently and olanzapine blocked the stereotypy and climbing induced by apomorphine at doses that did not induce catalepsy.