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    Jaceosidin
    Information
    CAS No. 18085-97-7 Price $198 / 20mg
    Catalog No.CFN90386Purity>=98%
    Molecular Weight330.29Type of CompoundFlavonoids
    FormulaC17H14O7Physical DescriptionYellow powder
    Download Manual    COA    MSDS    SDFSimilar structuralComparison (Web)
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    Jaceosidin Description
    Source: The herbs of Artemisia arctica
    Biological Activity or Inhibitors: 1. Jaceosidin has anti-oxidative activity.
    2. Jaceosidin has anti-inflammatory activity, also a microglial inhibitor with anti-neuroinflammation activity.
    3. Jaceosidin has anticancer activity, modulates the ERK/ATM/Chk1/2 pathway, leading to inactivation of the Cdc2-cyclin B1 complex, followed by G2/M cell cycle arrest in endometrial cancer cells.
    4. Jaceosidin has immunosuppressive effect through inhibiting T cell proliferation and activation, which is closely associated with its potent down-regulation of the IFN-γ/STAT1/T-bet signaling pathway.
    5. The pharmacokinetics of Jaceosidin may be dramatically affected by polymorphic CYP1A2, UGT1A1, and UGT1A7 responsible for the metabolism of Jaceosidin or by the coadministration of relevant CYP1A2 or UGT inhibitors or inducers.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, 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.
    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 3.0276 mL 15.1382 mL 30.2764 mL 60.5528 mL 75.6911 mL
    5 mM 0.6055 mL 3.0276 mL 6.0553 mL 12.1106 mL 15.1382 mL
    10 mM 0.3028 mL 1.5138 mL 3.0276 mL 6.0553 mL 7.5691 mL
    50 mM 0.0606 mL 0.3028 mL 0.6055 mL 1.2111 mL 1.5138 mL
    100 mM 0.0303 mL 0.1514 mL 0.3028 mL 0.6055 mL 0.7569 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.
    Jaceosidin References Information
    Citation [1]

    Exp Biol Med (Maywood). 2014 Oct;239(10):1325-34.

    Jaceosidin, a natural flavone, promotes angiogenesis via activation of VEGFR2/FAK/PI3K/AKT/NF-κB signaling pathways in endothelial cells.[Pubmed: 24939823 ]
    Angiogenesis, the growth of new blood vessels from pre-existing vasculature, plays an important role in physiological and pathological processes such as embryonic development wound healing and revascularization of tissues after exposure to ischemia. We investigated the effects of Jaceosidin, a main constituent of medicinal herbs of the genus Artemisia, on angiogenesis and signaling pathways in endothelial cells. Jaceosidin stimulated proliferation, migration and tubulogenesis of ECs as well as ex vivo sprouting from aorta rings, which are phenomena typical of angiogenesis. Jaceosidin activated vascular endothelial growth factor receptor 2 (VEGFR2, FLk-1/KDR) and angiogenic signaling molecules such as focal adhesion kinase, phosphatidylinositol 3-kinase, and its downstream target, the serine-threonine kinase AKTWe also demonstrated that Jaceosidin activated the NF-κB-driven expression of a luciferase reporter gene and NF-κB binding to DNA. Jaceosidin-induced proliferation and migration of human umbilical vascular endothelial cells were strongly inhibited by the phosphatidylinositol 3-kinase inhibitor LY294002 and NF-κB inhibitor BAY11-7082, indicating that the PI3K/AKT/NF-κB signaling pathway is involved in Jaceosidin-induced angiogenesis. Our results suggest that Jaceosidin stimulates angiogenesis by activating the VEGFR2/FAK/PI3K/AKT/NF-κB signaling pathway and that it may be useful in developing angiogenic agents to promote the growth of collateral blood vessels in ischemic tissues.
    Citation [2]

    Food Chem Toxicol. 2013 May;55:214-21.

    Jaceosidin, isolated from dietary mugwort (Artemisia princeps), induces G2/M cell cycle arrest by inactivating cdc25C-cdc2 via ATM-Chk1/2 activation.[Pubmed: 23274058]
    Jaceosidin, a flavonoid derived from Artemisia princeps (Japanese mugwort), has been shown to inhibit the growth of several human cancer cells, However, the exact mechanism for the cytotoxic effect of Jaceosidin is not completely understood. In this study, we investigated the molecular mechanism involved in the antiproliferative effect of Jaceosidin in human endometrial cancer cells. We demonstrated that Jaceosidin is a more potent inhibitor of cell growth than cisplatin in human endometrial cancer cells. In contrast, Jaceosidin-induced cytotoxicity in normal endometrial cells was lower than that observed for cisplatin. Jaceosidin induced G2/M phase cell cycle arrest and modulated the levels of cyclin B and p-Cdc2 in Hec1A cells. Knockdown of p21 using specific siRNAs partially abrogated Jaceosidin-induced cell growth inhibition. Additional mechanistic studies revealed that Jaceosidin treatment resulted in an increase in phosphorylation of Cdc25C and ATM-Chk1/2. Ku55933, an ATM inhibitor, reversed Jaceosidin-induced cell growth inhibition, in part. Moreover, Jaceosidin treatment resulted in phosphorylation of ERK, and pretreatment with the ERK inhibitor, PD98059, attenuated cell growth inhibition by Jaceosidin. These data suggest that Jaceosidin, isolated from Japanese mugwort, modulates the ERK/ATM/Chk1/2 pathway, leading to inactivation of the Cdc2-cyclin B1 complex, followed by G2/M cell cycle arrest in endometrial cancer cells.
    Citation [3]

    Phytother Res. 2013 Mar;27(3):404-11.

    Natural flavone jaceosidin is a neuroinflammation inhibitor.[Pubmed: 22619052]
    Jaceosidin is a naturally occurring flavone with pharmacological activity. Jaceosidin, as one of the major constituents of the medicinal herbs of the genus Artemisia, has been shown to exert anticancer, anti-oxidative, anti-inflammatory, and immunosuppressive effects. This study was undertaken to determine the effect of Jaceosidin on microglia and neuroinflammation. Microglia are the innate immune cells in the central nervous system, and they play a central role in the initiation and maintenance of neuroinflammation. We report that Jaceosidin inhibits inflammatory activation of microglia, reducing nitric oxide (NO) production and proinflammatory cytokine expression. IC50 for NO inhibition was 27 ± 0.4 μM. The flavone also attenuated microglial neurotoxicity in the microglia/neuroblastoma co-culture. Systemic injection of Jaceosidin ameliorated neuroinflammation in the mouse model of experimental allergic encephalomyelitis. These results indicate that plant flavone Jaceosidin is a microglial inhibitor with anti-neuroinflammation activity.
    Citation [4]

    Arch Pharm Res. 2010 Dec;33(12):1985-96.

    In vitro metabolism of jaceosidin and characterization of cytochrome P450 and UDP-glucuronosyltransferase enzymes in human liver microsomes.[Pubmed: 21191764]
    Jaceosidin is an active component in Artemisia species as well as Eupatorium species and it exhibits antiallergic, anticancer, antioxidant, anti-inflammatory, and antimutagenic activities. Jaceosidin was metabolized to Jaceosidin glucuronide, 6-O-desmethylJaceosidin, hydroxyJaceosidin, 6-O-desmethylJaceosidin glucuronide, and hydroxyJaceosidin glucuronide in human liver microsomes. This study characterized the human liver cytochrome P450 (CYP) and UDPglucuronosyltransferase (UGT) enzymes responsible for the metabolism of Jaceosidin. CYP1A2 was identified as the major enzyme responsible for the formation of 6-O-desmethylJaceosidin and hydroxyJaceosidin from Jaceosidin on the basis of a combination of correlation analysis and experiments including immuno-inhibition, chemical inhibition in human liver microsomes, and metabolism by human cDNA-expressed CYP enzymes. Jaceosidin glucuronidation was catalyzed by UGT1A1, UGT1A3, UGT1A7, UGT1A8, UGT1A9, and UGT1A10. These results suggest that the pharmacokinetics of Jaceosidin may be dramatically affected by polymorphic CYP1A2, UGT1A1, and UGT1A7 responsible for the metabolism of Jaceosidin or by the coadministration of relevant CYP1A2 or UGT inhibitors or inducers.
    Citation [5]

    Eur J Pharmacol. 2011 Jan 25;651(1-3):205-11.

    Jaceosidin inhibits contact hypersensitivity in mice via down-regulating IFN-γ/STAT1/T-bet signaling in T cells.[Pubmed: 21093428]
    In the present study, we aimed to investigate the immunosuppressive activity of Jaceosidin, a flavone isolated from Artemisia vestita, on T lymphocytes both in vitro and in vivo, and further explore its potential molecular mechanism. Jaceosidin exerted a significant inhibition on the T cell proliferation and activation induced by concanavalin A (Con A) in a concentration-dependent manner and it also inhibited the secretion of the proinflammatory cytokines such as IL-2, TNF-α and IFN-γ of activated T cells. Further study showed that Jaceosidin down-regulated STAT1 activation and T-bet expression in activated T cells. Moreover, in order to investigate the immunosuppressive effect of Jaceosidin in vivo, the picryl chloride (PCl)-induced ear contact dermatitis model was performed on BALB/c mice. Jaceosidin significantly ameliorated PCl-induced ear swelling in a dose-dependent manner, which was due to its inhibition of the STAT1/T-bet signaling pathway. In summary, these findings suggest that Jaceosidin exerts its immunosuppressive effect both in vitro and in vivo through inhibiting T cell proliferation and activation, which is closely associated with its potent down-regulation of the IFN-γ/STAT1/T-bet signaling pathway.