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    Myricitrin
    Information
    CAS No. 17912-87-7 Price $40 / 20mg
    Catalog No.CFN99840Purity>=98%
    Molecular Weight464.4 Type of CompoundFlavonoids
    FormulaC21H20O12Physical DescriptionYellow powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Myricitrin exhibits hepatoprotective, anti-inflammatory,antioxidant, anti-allergic, antinociception, anxiolytic-like, and antipsychotic-like effects. Myricitrin can be used as a drug candidate for the treatment of cardiovascular diseases, by effectively protecting cells from ox-LDL-induced endothelial cell apoptosis and reducing atherosclerotic plaque formation. Myricitrin is also a nitric oxide (NO) and protein kinase C (PKC) inhibitor that has central nervous system activity.
    Targets: LDL | PKC | NO | NOS | ROS | STAT | PI3K | Akt | NOS | IAP | COX | TNF-α | TGF-β/Smad | P450 (e.g. CYP17)
    In vitro:
    Nat Prod Commun. 2015 Jan;10(1):83-8.
    Phytochemical profile of the aerial parts of Sedum sediforme and anti-inflammatory activity of myricitrin.[Pubmed: 25920226]
    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.
    METHODS AND RESULTS:
    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.
    CONCLUSIONS:
    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.
    Biochem Biophys Res Commun. 2015 Mar 6;458(2):227-33.
    Myricitrin alleviates MPP⁺-induced mitochondrial dysfunction in a DJ-1-dependent manner in SN4741 cells.[Pubmed: 25623535]
    Oxidative stress and mitochondrial dysfunction have been linked to Parkinson's disease. DJ-1 is a recessive familial PD gene involved in antioxidative function and mitochondrial maintenance. Myricitrin, a flavanoid isolated from the root bark of Myrica cerifera, has potent antioxidative properties.
    METHODS AND RESULTS:
    In the present study, we investigated the protective effects of Myricitrin against MPP(+)-induced mitochondrial dysfunction in SN4741 cells and attempted to elucidate the mechanisms underlying this protection. The results showed that incubating SN4741 cells with Myricitrin significantly reduced cell death induced by the neurotoxin MPP(+). Furthermore, Myricitrin protected cells from MPP(+)-induced effects on mitochondrial morphology and function. However, these protective effects were lost under DJ-1-deficient conditions.
    CONCLUSIONS:
    Thus, our results suggest that Myricitrin alleviates MPP(+)-induced mitochondrial dysfunction and increases cell viability via DJ-1, indicating that Myricitrin is a potential beneficial agent for age-related neurodegenerative diseases, particularly Parkinson's disease.
    In vivo:
    Vascul Pharmacol. 2015 Apr 4.
    Myricitrin attenuates endothelial cell apoptosis to prevent atherosclerosis: An insight into PI3K/Akt activation and STAT3 signaling pathways.[Pubmed: 25849952]
    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.
    METHODS AND RESULTS:
    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.
    CONCLUSIONS:
    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.
    Nat Prod Res. 2011 Feb;25(4):374-80.
    Anti-allergic effect of the flavonoid myricitrin from Myrica rubra leaf extracts in vitro and in vivo.[Pubmed: 21328132 ]
    Flavonoids are ingested by the general population as anti-oxidant and anti-inflammatory agents.
    METHODS AND RESULTS:
    In this study, we investigated the effects of Myricitrin, a flavonoid rich in Myrica rubra leaf, upon anti-inflammatory action. Myrica rubra leaf extracts inhibited pro-inflammatory TNFα production in a macrophage cell line, Raw264.7 cells. We observed that the serum IgE levels in the leaf extract-treated DO11.10, a mouse allergy model, were down-regulated. HPLC was performed to demonstrate that M. rubra leaf extracts contain a large amount of Myricitrin. We observed an inhibitory effect of HPLC-purified Myricitrin on TNFα production in Raw264.7 cells.
    CONCLUSIONS:
    Thus, Myricitrin may be of potential interest in the management of inflammatory conditions.
    Myricitrin Description
    Source: The root barks of Myrica cerifera L.
    Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.1533 mL 10.7666 mL 21.5332 mL 43.0663 mL 53.8329 mL
    5 mM 0.4307 mL 2.1533 mL 4.3066 mL 8.6133 mL 10.7666 mL
    10 mM 0.2153 mL 1.0767 mL 2.1533 mL 4.3066 mL 5.3833 mL
    50 mM 0.0431 mL 0.2153 mL 0.4307 mL 0.8613 mL 1.0767 mL
    100 mM 0.0215 mL 0.1077 mL 0.2153 mL 0.4307 mL 0.5383 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Protocol
    Kinase Assay:
    Prog Neuropsychopharmacol Biol Psychiatry. 2011 Aug 15;35(7):1636-44.
    Myricitrin, a nitric oxide and protein kinase C inhibitor, exerts antipsychotic-like effects in animal models.[Pubmed: 21689712 ]
    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.
    METHODS AND RESULTS:
    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.
    Animal Research:
    Chem Biol Interact. 2015 Mar 25;230:21-9.
    Myricitrin exhibits antioxidant, anti-inflammatory and antifibrotic activity in carbon tetrachloride-intoxicated mice.[Pubmed: 25656916]
    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.
    METHODS AND RESULTS:
    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.
    CONCLUSIONS:
    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.
    J Pharmacol Exp Ther. 2006 Feb;316(2):789-96.
    Analysis of the antinociceptive effect of the flavonoid myricitrin: evidence for a role of the L-arginine-nitric oxide and protein kinase C pathways.[Pubmed: 16260583 ]
    The present study investigated the antinociceptive effects of the flavonoid Myricitrin in chemical behavioral models of pain in mice and rats.
    METHODS AND RESULTS:
    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.
    CONCLUSIONS:
    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.