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    Hyperoside
    Information
    CAS No. 482-36-0 Price $50 / 20mg
    Catalog No.CFN98754Purity>=98%
    Molecular Weight464.4 Type of CompoundFlavonoids
    FormulaC21H20O12Physical DescriptionYellow powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Hyperoside, a naturally occuring flavonoid compound, exerts multiple bioactivities, including myocardial protection, anti-redox, neuroprotective, antifungal, hepatoprotective, anti-inflammatory and antioxidative effects. Hyperoside is a potent natural activator of Nur77 receptor, and a potent selective CYP2D6 inhibitor; it inhibited the HMGB1 signaling pathway, and inhibited the PI3K/Akt/Bad/Bcl XL -regulated mitochondrial apoptotic pathway. Hyperoside is a strong inhibitor of HBsAg and HBeAgsecretion in 2.2.15 cells and DHBV-DNA levels in the HBV-infected duck model.
    Targets: ERK | cAMP | NF-kB | TNF-α | Akt | IL Receptor | JNK | P450 (e.g. CYP17) | HBV | Bcl-2/Bax | PI3K | Beta Amyloid | PARP | TNF-α | NOS | COX | HO-1 | Nrf2
    In vitro:
    Int J Mol Sci. 2013 Nov 18;14(11):22697-707.
    Hyperoside downregulates the receptor for advanced glycation end products (RAGE) and promotes proliferation in ECV304 cells via the c-Jun N-terminal kinases (JNK) pathway following stimulation by advanced glycation end-products in vitro.[Pubmed: 24252909]
    Hyperoside is a major active constituent in many medicinal plants which are traditionally used in Chinese medicines for their neuroprotective, anti-inflammatory and antioxidative effects. The molecular mechanisms underlying these effects are unknown.
    METHODS AND RESULTS:
    In this study, quiescent ECV304 cells were treated in vitro with advanced glycation end products (AGEs) in the presence or absence of Hyperoside. The results demonstrated that AGEs induced c-Jun N-terminal kinases (JNK) activation and apoptosis in ECV304 cells. Hyperoside inhibited these effects and promoted ECV304 cell proliferation. Furthermore, Hyperoside significantly inhibited RAGE expression in AGE-stimulated ECV304 cells, whereas knockdown of RAGE inhibited AGE-induced JNK activation. These results suggested that AGEs may promote JNK activation, leading to viability inhibition of ECV304 cells via the RAGE signaling pathway. These effects could be inhibited by Hyperoside.
    CONCLUSIONS:
    Our findings suggest a novel role for Hyperoside in the treatment and prevention of diabetes.
    J Agric Food Chem. 2005 Jan 12;53(1):32-7.
    Antifungal activity of camptothecin, trifolin, and hyperoside isolated from Camptotheca acuminata.[Pubmed: 15631505]
    Leaf spots and root rots are major fungal diseases in Camptotheca acuminata that limit cultivation of the plant for camptothecin (CPT), a promising anticancer and antiviral alkaloid.
    METHODS AND RESULTS:
    Bioassays showed that pure CPT and flavonoids (trifolin and Hyperoside) isolated from Camptotheca effectively control fungal pathogens in vitro, including Alternaria alternata, Epicoccum nigrum, Pestalotia guepinii, Drechslera sp., and Fusarium avenaceum, although antifungal activity of these compounds in the plant is limited. CPT inhibited mycelial growth by approximately 50% (EC50) at 10-30 microg/mL and fully inhibited growth at 75-125 microg/mL. The flavonoids were less effective than CPT at 50 microg/mL, particularly within 20 days after treatment, but more effective at 100 or 150 microg/mL.
    CONCLUSIONS:
    CPT, trifolin, and Hyperoside may serve as leads for the development of fungicides.
    Eur J Pharmacol. 2011 Dec 15;672(1-3):45-55.
    Hyperoside protects primary rat cortical neurons from neurotoxicity induced by amyloid β-protein via the PI3K/Akt/Bad/Bcl(XL)-regulated mitochondrial apoptotic pathway.[Pubmed: 21978835 ]
    Amyloid β-protein (Aβ), which is deposited in neurons as neurofibrillary tangles, is known to exert cytotoxic effects by inducing mitochondrial dysfunction. Additionally, the PI3K/Akt-mediated interaction between Bad and Bcl(XL) plays an important role in maintaining mitochondrial integrity. However, the application of therapeutic drugs, especially natural products in Alzheimer's disease therapy via PI3K/Akt/Bad/Bcl(XL)-regulated mitochondrial apoptotic pathway has not aroused extensive attention.
    METHODS AND RESULTS:
    In the present study, we investigated the neuroprotective effects of Hyperoside, a bioactive flavonoid compound from Hypericum perforatum, on Aβ(25-35)-induced primary cultured cortical neurons, and also examined the potential cellular signaling mechanism for Aβ detoxication. Our results showed that treatment with Hyperoside significantly inhibited Aβ(25-35)-induced cytotoxicity and apoptosis by reversing Aβ-induced mitochondrial dysfunction, including mitochondrial membrane potential decrease, reactive oxygen species production, and mitochondrial release of cytochrome c. Further study indicated that Hyperoside can activate the PI3K/Akt signaling pathway, resulting in inhibition of the interaction between Bad and Bcl(XL), without effects on the interaction between Bad and Bcl-2. Furthermore, Hyperoside inhibited mitochondria-dependent downstream caspase-mediated apoptotic pathway, such as that involving caspase-9, caspase-3, and poly ADP-ribose polymerase (PARP).
    CONCLUSIONS:
    These results demonstrate that Hyperoside can protect Aβ-induced primary cultured cortical neurons via PI3K/Akt/Bad/Bcl(XL)-regulated mitochondrial apoptotic pathway, and they raise the possibility that Hyperoside could be developed into a clinically valuable treatment for Alzheimer's disease and other neuronal degenerative diseases associated with mitochondrial dysfunction.
    In vivo:
    Inflammation. 2015 Apr;38(2):784-99.
    Anti-inflammatory effects of hyperoside in human endothelial cells and in mice.[Pubmed: 25097077]
    High-mobility group box 1 (HMGB1) was recently shown to be an important extracellular mediator of systemic inflammation, and endothelial cell protein C receptor (EPCR) has been shown to be involved in vascular inflammation. Hyperoside is an active compound isolated from Rhododendron brachycarpum G. Don (Ericaceae) that was reported to have anti-oxidant, anti-hyperglycemic, anti-cancer, and anti-coagulant activities.
    METHODS AND RESULTS:
    Here, we show, for the first time, the anti-septic effects of Hyperoside in HMGB1-mediated inflammatory responses and on the shedding of EPCR in vitro and in vivo. The data showed that Hyperoside posttreatment suppressed lipopolysaccharide (LPS)-mediated release of HMGB1 and HMGB1-mediated cytoskeletal rearrangement. Hyperoside also inhibited HMGB1-mediated hyperpermeability and leukocyte migration in septic mice and phorbol-12-myristate 13-acetate (PMA) of cecal ligation and puncture (CLP)-induced EPCR shedding. In addition, Hyperoside inhibited the production of tumor necrosis factor-α (TNF-α) and the HMGB1-mediated activation of Akt, nuclear factor-κB (NF-κB), and extracellular regulated kinase (ERK) 1/2 in HUVECs. Hyperoside also reduced the CLP-induced release of HMGB1, the production of interleukin (IL)-1β, and septic mortality.
    CONCLUSIONS:
    Collectively, these results suggest Hyperoside as a candidate therapeutic agent for the treatment of vascular inflammatory diseases via inhibition of the HMGB1 signaling pathway.
    Hyperoside Description
    Source: The herbs of Hypericum perforatum 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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    Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

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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:
    Biochem Pharmacol. 2014 Dec 15;92(4):590-8.
    Induction of Nur77 by hyperoside inhibits vascular smooth muscle cell proliferation and neointimal formation.[Pubmed: 25316569]
    Nur77 is an orphan nuclear receptor that belongs to the nuclear receptor 4A (NR4A) subfamily, which has been implicated in a variety of biological events, such as cell apoptosis, proliferation, inflammation, and metabolism. Activation of Nur77 has recently been shown to be beneficial for the treatment of cardiovascular and metabolic diseases. The purpose of this study is to identify novel natural Nur77 activators and investigate their roles in preventing vascular diseases.
    METHODS AND RESULTS:
    By measuring Nur77 expression using quantitative RT-PCR, we screened active ingredients extracted from Chinese herb medicines with beneficial cardiovascular effects. Hyperoside (quercetin 3-D-galactoside) was identified as one of the potent activators for inducing Nur77 expression and activating its transcriptional activity in vascular smooth muscle cells (VSMCs). We demonstrated that Hyperoside, in a time and dose dependent manner, markedly increased the expression of Nur77 in rat VSMCs, with an EC50 of ~0.83 μM. Mechanistically, we found that Hyperoside significantly increased the phosphorylation of ERK1/2 MAP kinase and its downstream target cAMP response element-binding protein (CREB), both of which contributed to the Hyperoside-induced Nur77 expression in rat VSMCs. Moreover, through activation of Nur77 receptor, Hyperoside markedly inhibited both vascular smooth muscle cell proliferation in vitro and the carotid artery ligation-induced neointimal formation in vivo.
    CONCLUSIONS:
    These findings demonstrate that Hyperoside is a potent natural activator of Nur77 receptor, which can be potentially used for prevention and treatment of occlusive vascular diseases.
    Food Chem Toxicol. 2013 Sep;59:549-53.
    Selective inhibition of the cytochrome P450 isoform by hyperoside and its potent inhibition of CYP2D6.[Pubmed: 23835282]
    Hyperoside, quercetin-3-O-galactoside, is a flavonoid isolated from Oenanthe javanica.
    METHODS AND RESULTS:
    In the present study, we investigated potential herb-drug inhibitory effects of Hyperoside on nine cytochrome P450 (CYP) isoforms in pooled human liver microsomes (HLMs) and human recombinant cDNA expressed CYP using a cocktail probe assay. Hyperoside strongly inhibited CYP2D6-catalyzed dextromethorphan O-demethylation, with IC₅₀ values of 1.2 and 0.81 μM after 0 and 15 min of preincubation, and a Ki value of 2.01 μM in HLMs, respectively. Hyperoside strongly decreased CYP2D6 activity dose-, but not time-, dependently in HLMs. In addition, the Lineweaver-Burk and Secondary plots for the inhibition of CYP2D6 in HLMs fitted a competitive inhibition mode. Furthermore, Hyperoside decreased CYP2D6-catalyzed dextromethorphan O-demethylation activity of human recombinant cDNA-expressed CYP2D6, with an IC₅₀ value of 3.87 μM. However, other CYPs were not inhibited significantly by Hyperoside.
    CONCLUSIONS:
    In conclusion, our data demonstrate that Hyperoside is a potent selective CYP2D6 inhibitor in HLMs, and suggest that Hyperoside might cause herb-drug interactions when co-administrated with CYP2D substrates.
    Cell Research:
    Acta Pharmacol Sin. 2007 Mar;28(3):404-9.
    In vivo and in vitro antiviral activity of hyperoside extracted from Abelmoschus manihot (L) medik.[Pubmed: 17303004 ]
    To assess the anti-hepatitis B virus (HBV) effect of Hyperoside extracted from Abelmoschus manihot (L) medik.
    METHODS AND RESULTS:
    The human hepatoma Hep G2.2.15 cell culture system and duck hepatitis B virus (DHBV) infection model were used as in vivo and in vitro models to evaluate the anti-HBV effects. In the cell model, the 50% toxic concentration of Hyperoside was 0.115 g/L; the maximum nontoxic concentration was 0.05 g/L. On the maximum nontoxic concentrations, the inhibition rates of Hyperoside on HBeAg and HBsAg in the 2.2.15 cells were 86.41% and 82.27% on d 8, respectively. In the DHBV infection model, the DHBV-DNA levels decreased significantly in the treatment of 0.05 g x kg(-1 ) x d(-1 ) and 0.10 g x kg(-1) x d(-1) dosage groups of Hyperoside (P<0.01). The inhibition of the peak of viremia was at the maximum at the dose of 0.10 g x kg(-1 ) x d(-1) and reached 60.79% on d 10 and 69.78% on d 13, respectively.
    CONCLUSIONS:
    These results suggested that Hyperoside is a strong inhibitor of HBsAg and HBeAg secretion in 2.2.15 cells and DHBV-DNA levels in the HBV-infected duck model.
    Animal Research:
    J Nat Prod. 2011 May 27;74(5):1055-60.
    Protective effects of hyperoside against carbon tetrachloride-induced liver damage in mice.[Pubmed: 21428416 ]
    In this study, the hepatoprotective effects of Hyperoside (1), a flavonoid glycoside isolated from Artemisia capillaris, have been examined against carbon tetrachloride (CCl4)-induced liver injury.
    METHODS AND RESULTS:
    Mice were treated intraperitoneally with vehicle or 1 (50, 100, and 200 mg·kg(-1)) 30 min before and 2 h after CCl4 (20 μL·kg(-1)) injection. Levels of serum aminotransferases were increased 24 h after CCl4 injection, and these increases were attenuated by 1. Histological analysis showed that 1 prevented portal inflammation, centrizonal necrosis, and Kupffer cell hyperplasia. Lipid peroxidation was increased and hepatic glutathione content was decreased significantly after CCl4 treatment, and these changes were reduced by administration of 1. Protein and mRNA expression of tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and heme oxygenase-1 (HO-1) and nuclear protein expression of nuclear factor erythroid 2-related factor 2 (Nrf2) significantly increased after CCl4 injection. Compound 1 suppressed TNF-α, iNOS, and COX-2 protein and mRNA expression and augmented HO-1 protein and mRNA expression and Nrf2 nuclear protein expression.
    CONCLUSIONS:
    These results suggest that 1 has protective effects against CCl4-induced acute liver injury, and this protection is likely due to enhancement of the antioxidative defense system and suppression of the inflammatory response.