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    Ginkgolide A
    Information
    CAS No. 15291-75-5 Price $70 / 20mg
    Catalog No.CFN99638Purity>=98%
    Molecular Weight408.4 Type of CompoundDiterpenoids
    FormulaC20H24O9Physical DescriptionPowder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Ginkgolide A is a platelet-activating factor antagonist, it can inhibit the neurotoxicity of prions or amyloid-beta1-42, may be relevant treatments for prion or Alzheimer's diseases.Ginkgolide A has neuroprotective, and anxiolytic-like effects, it is widely used for the treatment of cardiovascular diseases and diabetic vascular complications, which might be achieved through regulating the STAT3-mediated pathway.
    Targets: STAT | IL Receptor | PI3K | Akt | GSK-3 | P450 (e.g. CYP17) | Caspase | Beta Amyloid
    In vitro:
    Int Immunopharmacol. 2015 Apr;25(2):242-8.
    Ginkgolide A reduces inflammatory response in high-glucose-stimulated human umbilical vein endothelial cells through STAT3-mediated pathway.[Pubmed: 25681539]
    High-glucose-induced low-grade inflammation has been regarded as a key event in the onset and progression of endothelial dysfunction in diabetic vascular complications. Ginkgolide A (GA), a major compound from Ginkgo biloba extract, is widely used for the treatment of cardiovascular diseases and diabetic vascular complications. Here, its effect on high-glucose-stimulated vascular inflammation in human umbilical vein endothelial cells (HUVECs) was investigated.
    METHODS AND RESULTS:
    In the present study, the optimal stimulation conditions for HUVECs were screened for inducing endothelial inflammation, namely, high glucose at the concentration of 30mM for continuous 8h. The endothelial production of high-glucose-induced interleukin (IL)-4, IL-6, IL-13 and signal transducer and activator of transcription-3 (STAT-3) phosphorylation were significantly inhibited by the pretreatment with GA at concentrations of 10, 15 and 20μM based on enzyme-linked immunosorbent assay (ELISA), western blot or/and RT-PCR experiments. These senescent alterations induced by high glucose were significantly attenuated by the specific STAT3 inhibitor S3I-201 at the concentration of 20μM. Furthermore, the phosphorylation of STAT3, IL-4, IL-6, IL-13 and intercellular cell adhesion molecule-1 (ICAM-1) protein as well as mRNA levels were attenuated by the pretreatment of cells with STAT3 siRNA. Our results demonstrated that GA improved high-glucose-caused low-grade vascular inflammation, which might be achieved through regulating the STAT3-mediated pathway.
    CONCLUSIONS:
    These findings indicated that GA might be a promising candidate for attenuating vascular inflammation in diabetic vascular complications.
    In vivo:
    J Nat Prod. 2003 Oct;66(10):1333-7.
    An anxiolytic-like effect of Ginkgo biloba extract and its constituent, ginkgolide-A, in mice.[Pubmed: 14575433 ]
    The anxiolytic-like effects of Ginkgo biloba extract (GBE) and its four terpenoid components (Ginkgolide A, ginkgolide B, ginkgolide C, and bilobalide) were assessed using the elevated plus-maze test in mice.
    METHODS AND RESULTS:
    Administration of GBE as a single oral dose (0.5 or 1 g/kg, po) caused a state of suppressed motor activity and, thus, shortened the time spent in the open-sided arms. However, when GBE (0.063-1 g/kg, po) was administered daily for 7 days and the plus-maze test was carried out 24 h after the final administration, the time spent in the open-sided arms was prolonged, with the peak anxiolytic-like effect at 0.125 g/kg. A combination of seven-day administration of GBE (0.125 g/kg) and a single dose of diazepam (1 mg/ kg, po, 10 min before testing) enhanced the anxiolytic-like effect. Flumazenil (0.3 mg/kg, ip, 10 min before testing) blocked the effect of diazepam, but not of GBE. Daily administration of Ginkgolide A (1 or 2 mg/kg, po) resulted in an anxiolytic-like effect by the third treatment, with the maximal effect observed after the fifth administration. Neither ginkgolide B, ginkgolide C, nor bilobalide produced any anxiolytic-like effects. At doses higher than 0.5 g/kg, GBE not only inhibited motor activity but also suppressed active avoidance behavior, reduced caffeine-induced stimulation, and enhanced pentobarbital-induced sleep, while Ginkgolide A (up to 20 mg/kg) did not exhibit these effects. Diazepam (1 mg/kg) is known to enhance pentobarbital-induced sleep.
    CONCLUSIONS:
    These results suggest that GBE produces a significant anxiolytic-like effect following repeated administration and that Ginkgolide A is most likely responsible for this effect. There are also indications that although GBE exerts a sedative effect at comparatively higher doses, Ginkgolide A has a relatively weak tendency to produce benzodiazepine-like side effects.
    Ginkgolide A Description
    Source: The leaves of Ginkgo biloba L.
    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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    Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

    Cell. 2018 Jan 11;172(1-2):249-261.e12.
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    J Cell Biochem. 2018 Feb;119(2):2231-2239.
    doi: 10.1002/jcb.26385.

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    Phytomedicine. 2018 Feb 1;40:37-47.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.4486 mL 12.2429 mL 24.4858 mL 48.9716 mL 61.2145 mL
    5 mM 0.4897 mL 2.4486 mL 4.8972 mL 9.7943 mL 12.2429 mL
    10 mM 0.2449 mL 1.2243 mL 2.4486 mL 4.8972 mL 6.1214 mL
    50 mM 0.049 mL 0.2449 mL 0.4897 mL 0.9794 mL 1.2243 mL
    100 mM 0.0245 mL 0.1224 mL 0.2449 mL 0.4897 mL 0.6121 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:
    Toxicol Appl Pharmacol. 2006 Dec 1;217(2):225-33.
    Ginkgolide A contributes to the potentiation of acetaminophen toxicity by Ginkgo biloba extract in primary cultures of rat hepatocytes.[Pubmed: 17045319]
    The present cell culture study investigated the effect of Ginkgo biloba extract pretreatment on acetaminophen toxicity and assessed the role of Ginkgolide A and cytochrome P450 3A (CYP3A) in hepatocytes isolated from adult male Long-Evans rats provided ad libitum with a standard diet.
    METHODS AND RESULTS:
    Acetaminophen (7.5-25 mM for 24 h) conferred hepatocyte toxicity, as determined by the lactate dehydrogenase (LDH) assay. G. biloba extract alone increased LDH leakage in hepatocytes at concentrations > or =75 mug/ml and > or =750 mug/ml after a 72 h and 24 h treatment period, respectively. G. biloba extract (25 or 50 mug/ml once every 24 h for 72 h) potentiated LDH leakage by acetaminophen (10 mM for 24 h; added at 48 h after initiation of extract pretreatment). The effect was confirmed by a decrease in [(14)C]-leucine incorporation. At the level present in a modulating concentration (50 mug/ml) of the extract, Ginkgolide A (0.55 mug/ml), which increased CYP3A23 mRNA levels and CYP3A-mediated enzyme activity, accounted for part but not all of the potentiating effect of the extract on acetaminophen toxicity. This occurred as a result of CYP3A induction by Ginkgolide A because triacetyloleandomycin (TAO), a specific inhibitor of CYP3A catalytic activity, completely blocked the effect of Ginkgolide A. Ginkgolide B, ginkgolide C, ginkgolide J, quercetin, kaempferol, isorhamnetin, and isorhamnetin-3-O-rutinoside did not alter the extent of LDH leakage by acetaminophen.
    CONCLUSIONS:
    In summary, G. biloba pretreatment potentiated acetaminophen toxicity in cultured rat hepatocytes and Ginkgolide A contributed to this novel effect of the extract by inducing CYP3A.
    Cell Research:
    Planta Med. 2012 Aug;78(12):1337-41.
    Effects of ginkgolide A on okadaic acid-induced tau hyperphosphorylation and the PI3K-Akt signaling pathway in N2a cells.[Pubmed: 22700047]
    Alzheimer's disease is the most common form of dementia leading to the irreversible loss of neurons, and Tau hyperphosphorylation has an important role in the pathology of Alzheimer's disease. Ginkgolide A is one of the active components of Ginkgo biloba extracts which has been proven to have neuroprotective effects, but the effect of Ginkgolide A on Tau hyperphosphorylation has not yet been reported.
    METHODS AND RESULTS:
    In this study, the effects of Ginkgolide A on cell viability, Tau hyperphosphorylation, and the PI3K-Akt signaling pathway in N2a cell lines were explored, and methods such as the MTT assay, ELISA, and Western blots techniques were used. The results showed that Ginkgolide A could increase cell viability and suppress the phosphorylation level of Tau in cell lysates, meanwhile, GSK3β was inhibited with phosphorylation at Ser9. Moreover, treatment of the cells with Ginkgolide A promoted phosphorylation of PI3K and Akt,
    CONCLUSIONS:
    suggesting that the activation of the PI3K-Akt signaling pathway may be the mechanism for Ginkgolide A to prevent the intracellular accumulation of p-Tau induced by okadaic acid and to protect the cells from Tau hyperphosphorylation-related toxicity.