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    Panaxatriol
    Information
    CAS No. 32791-84-7 Price $50 / 20mg
    Catalog No.CFN99982Purity>=98%
    Molecular Weight476.73Type of CompoundTriterpenoids
    FormulaC30H52O4Physical DescriptionWhite powder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Panaxatriol is an inducer of thioredoxin-1 (Trx-1), which exhibits anti-inflammatory, hepatoprotective, anti-arrhythmic, and antioxidative activities. It has pluripharmacological properties in the protection against Parkinson's disease (PD) including enhancing antioxidant activity, acting as neurotrophic factor, modulating inflammation and inhibiting mitochondria-mediated apoptosis. Panaxatriol has been shown to be efficacious in the prevention and treatment of cerebrovascular diseases in China, it may activate endogenous cytoprotective mechanism against OGD-Rep induced oxidative injury via the activation of PI3K/Akt and Nrf2 signaling pathway.
    Targets: COX | Caspase | Nrf2 | HO-1 | PI3K | Akt | VEGFR | HSP (e.g. HSP90) | ATPase
    In vitro:
    J Ethnopharmacol. 2010 Feb 3;127(2):419-23.
    Panaxatriol saponins extracted from Panax notoginseng induces thioredoxin-1 and prevents 1-methyl-4-phenylpyridinium ion-induced neurotoxicity.[Pubmed: 19857566 ]
    Thioredoxin-1 has various biologic activities, including the control of redox balance and the inhibition of apoptosis. The current study was designed to examine the effects of Panaxatriol saponins (PTS) extracted from Panax notoginseng on thioredoxin-1 expression and 1-methyl-4-phenylpyridinium ion-induced injury.
    CONCLUSIONS:
    Using PC12 cells and Kunming mice, we test thioredoxin-1 expression after PTS treatment by Western blot. The protective effect of PTS against 1-methyl-4-phenylpyridinium ion-induced injury was assessed by MTT assay and LDH release assay. PTS induced thioredoxin-1 expression in vitro and in vivo, and attenuated 1-methyl-4-phenylpyridinium ion-induced cell death of PC12 cells.
    CONCLUSIONS:
    PTS is a new inducer of thioredoxin-1 and has a possible potential as a therapeutic agent for neurodegenerative diseases including Parkinson's disease.
    In vivo:
    Food Chem Toxicol. 2010 Jun;48(6):1516-20.
    The effects of ginseng total saponin, panaxadiol and panaxatriol on ischemia/reperfusion injury in isolated rat heart.[Pubmed: 20353807]
    The aim of the present study was to evaluate the protective effect of ginseng total saponin, panaxadiol and Panaxatriol, which are the major components of Panax ginseng, against myocardial ischemia/reperfusion (I/R) injury in isolated rat hearts.
    METHODS AND RESULTS:
    Rats were orally administered once a day with total saponin (20 mg/kg), panaxadiol (5 mg/kg) and Panaxatriol (5 mg/kg) for consecutive 7 days. On day 8, the hearts were isolated and perfused with Krebs-Henseleit bicarbonate buffer solution using Langendorff apparatus. After 30 min of global ischemia, hearts were reperfused for 30 min. Myocardial function, coronary flow and biochemical parameters, such as lactate dehydrogenase (LDH), creatine kinase (CK), adenosine triphosphate (ATP), malondialdehyde (MDA) and reduced glutathione (GSH) were measured. Total saponin and Panaxatriol significantly improved I/R-induced myocardial dysfunction by increasing left ventricular development pressure, (-dP/dt)/(+dP/dt) and time to contracture. Moreover, the increases in the levels of LDH, CK and MDA and the decrease in the levels of GSH were attenuated by total saponin and Panaxatriol. However, the ATP levels did not affected by total saponin, panaxadiol and Panaxatriol pretreatment.
    CONCLUSIONS:
    Our findings suggest that pretreatment with ginseng total saponin, especially Panaxatriol, ameliorates I/R-induced myocardial damage and this protection is caused by reducing oxidative stress.
    J Ethnopharmacol. 2011 Jan 27;133(2):448-53.
    Protective effect of panaxatriol saponins extracted from Panax notoginseng against MPTP-induced neurotoxicity in vivo.[Pubmed: 20951784 ]
    Panaxatriol saponins (PTS), the main constituents extracted from Panax notoginseng, a Chinese herbal medicine, has been shown to be an effective agent on various diseases. Our previous study has demonstrated that PTS is an inducer of thioredoxin-1 (Trx-1) and has a possible potential as a therapeutic agent for Parkinson's disease (PD). However, the effect of PTS on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity in vivo is unknown.
    METHODS AND RESULTS:
    Using locomotor activity test and traction test, we detected the effect of PTS on MPTP-induced behavioral impairment. Tyrosine hydroxylase, Trx-1, cyclooxygenase-2, pro-caspase-9, pro-caspase-12 and caspase-3 expressions in the anatomical region of substantia nigra pars compacta (SNc) were tested by Western blot. PTS provided neuroprotection against the loss of dopaminergic neurons and behavioral impairment caused by MPTP. MPTP-induced neuronal death in the SNc was suppressed by PTS through increasing Trx-1 expression, suppressing cyclooxygenase-2 over-expression and inhibiting mitochondria-mediated apoptosis.
    CONCLUSIONS:
    PTS, an inducer of Trx-1, has pluripharmacological properties in the protection against PD including enhancing antioxidant activity, acting as neurotrophic factor, modulating inflammation and inhibiting mitochondria-mediated apoptosis.
    Panaxatriol Description
    Source: The roots of Panax ginseng C. A. Mey.
    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.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.0976 mL 10.4881 mL 20.9762 mL 41.9525 mL 52.4406 mL
    5 mM 0.4195 mL 2.0976 mL 4.1952 mL 8.3905 mL 10.4881 mL
    10 mM 0.2098 mL 1.0488 mL 2.0976 mL 4.1952 mL 5.2441 mL
    50 mM 0.042 mL 0.2098 mL 0.4195 mL 0.839 mL 1.0488 mL
    100 mM 0.021 mL 0.1049 mL 0.2098 mL 0.4195 mL 0.5244 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:
    Oxid Med Cell Longev. 2014;2014:978034.
    Panaxatriol saponins attenuated oxygen-glucose deprivation injury in PC12 cells via activation of PI3K/Akt and Nrf2 signaling pathway.[Pubmed: 24955212]
    Panaxatriol saponins (PTS), the main components extracted from Panax notoginseng, have been shown to be efficacious in the prevention and treatment of cerebrovascular diseases in China. NF-E2-related factor 2 (Nrf2), a transcription factor regulating antioxidant and cytoprotective responses to oxidative stress, has received particular attention as a molecular target for pharmacological intervention of ischemic diseases. The aim of this study was to characterize the effect of PTS on the activation of Nrf2 signaling pathway and the potential role in its protective effect.
    METHODS AND RESULTS:
    We found that PTS induced heme oxygenase-1 (HO-1) expression in PC12 cells via activating Nrf2 signaling pathway. Phosphatidylinositol 3-kinase (PI3K)/Akt kinase was involved in the upstream of this PTS activated pathway. Moreover, combination of the main components in PTS significantly enhanced the expression of Nrf2 mediated phase II enzymes. Importantly, the protective effect of PTS against oxygen-glucose deprivation-reperfusion (OGD-Rep) induced cell death was significantly attenuated by PI3K inhibitor and antioxidant response element (ARE) decoy oligonucleotides, suggesting that both PI3K/Akt and Nrf2 signaling pathway are essential during this protective process.
    CONCLUSIONS:
    Taken together, our results suggest that PTS may activate endogenous cytoprotective mechanism against OGD-Rep induced oxidative injury via the activation of PI3K/Akt and Nrf2 signaling pathway.
    Animal Research:
    Zhongguo Zhong Yao Za Zhi. 2002 May;27(5):371-3.
    Protective effects and its mechanism of panaxatriol saponins isolated from Panax notoginseng on cerebral ischemia。[Pubmed: 12774330]
    To study the protective effects and its mechanism of Panaxatriol Saponins isolated from Panax notoginseng (PTS) on focal cerebral ischemia in rat brain.
    METHODS AND RESULTS:
    The influences of PTS on cerebral water content and three specific proteins (VEGF, HSP70 and transferrin) related with cerebral ischemia were studied with unilateral occlusion of the middle cerebral artery (MCAO) and Western Blot. PTS 12.5 mg.kg-1 i.p. x 7 d (5 d before MCAO and 2 d after MCAO) inhibited the increase of cerebral water content caused by MCAO and influenced contents of HSP70 and transferrin, but had no influence on VEGF protein level.
    CONCLUSIONS:
    PTS shows a protective effect on focal cerebral ischemia in rat brain by alleviating cerebral edema, up-regulating the expression of HSP70, down-regulating transferrin and maintaining blood-brain barrier.