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    Senkyunolide I
    CAS No. 94596-28-8 Price $318 / 20mg
    Catalog No.CFN99596Purity>=98%
    Molecular Weight224.3Type of CompoundMiscellaneous
    FormulaC12H16O4Physical DescriptionPowder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    According to end customer requirements, ChemFaces provide solvent format. This solvent format of product intended use: Signaling Inhibitors, Biological activities or Pharmacological activities.
    Size /Price /Stock 10 mM * 1 mL in DMSO / $120.4 / In-stock
    Other Packaging *Packaging according to customer requirements(100uL/well, 200uL/well and more), and Container use Storage Tube With Screw Cap
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  • Biological Activity
    Description: Senkyunolide I may be an active component of L. chuanxiong, traditionally used to treat migraine, it can protect rat brain against focal cerebral ischemia-reperfusion injury by up-regulating p-Erk1/2, Nrf2/HO-1 and inhibiting caspase 3, the neuroprotective mechanisms of itI are associated with its anti-oxidation and anti-apoptosis properties. Senkyunolide I can reduce the metamorphose damage of the RBC caused by ConA, the aggregation of the RBC can be alleviated by it.
    Targets: ERK | Nrf2 | HO-1 | Bcl-2/Bax | Caspase | 5-HT Receptor | NO
    In vitro:
    Lishizhen Medicine & Materia Medica Research, 2003, 14(12):738-9.
    Effects of Ferulic Acid,Senkyunolide H and Senkyunolide I on Erythrocytes[Reference: WebLink]
    To study the effects of Ferulic acid、Senkyunolide H and Senkyunolide I on erythrocytes deformability and aggregation.
    Deformability and aggregation of the dog RBC were evaluated through erythrocytes deformability experiment. Ferulic acid、Senkyunolide H and Senkyunolide I can reduce the metamorphose damage of the RBC caused by ConA.
    The aggregation experiment also has indicated that aggregation of the RBC can be alleviated by them.
    In vivo:
    Brain Res. 2015 Apr 24;1605:39-48.
    Senkyunolide I protects rat brain against focal cerebral ischemia-reperfusion injury by up-regulating p-Erk1/2, Nrf2/HO-1 and inhibiting caspase 3.[Pubmed: 25698615]
    Oxidative damage and apoptosis are critical factors contributing to neuronal death during a stroke. The aim of the present study was to evaluate the neuroprotective effects of Senkyunolide I (SEI) on focal cerebral ischemia-reperfusion (I/R) injury in rats, and investigate the underlying mechanisms.
    Male Sprague-Dawley rats were subjected to transient middle cerebral artery occlusion (tMCAO) for 2h, followed by 24h reperfusion, and then randomly assigned into four groups: Sham (sham-operated), Vehicle (tMCAO +normal saline), Senkyunolide I-L (tMCAO +SEI 36 mg/kg) and Senkyunolide I-H (tMCAO +SEI 72 mg/kg) groups. Senkyunolide I was administered intravenously, 15 min after occlusion. Neurological deficit, brain edema and infarct volume were detected after 24h of reperfusion. Histological structures of cortices and hippocampus were observed by hematoxylin and eosin staining. Biochemical indexes in the cortex were assayed by colorimetry. The impact of Senkyunolide I on the Nrf2-ARE-interaction was assayed using a luciferase reporter gene. Western blotting was performed to analysis the expressions of proteins related to anti-oxidation and apoptosis. Senkyunolide I administration significantly ameliorated the neurological deficit, reduced the infarct volume and brain edema, reversed the cerebral morphologic damage, decreased the levels of MDA and increased the activities of superoxide dismutase. Furthermore, the high dose Senkyunolide I could significantly activate the Nrf2/ARE pathway by up-regulating the phosphorylation of Erk1/2 and inducing Nrf2 nuclear translocation with enhanced HO-1 and NQO1 expressions. Additionally, treatment with Senkyunolide I remarkably promoted the ratio of Bcl-2/Bax and inhibited the expressions of cleaved caspase 3 and caspase 9.
    These results suggest that the neuroprotective mechanisms of Senkyunolide I are associated with its anti-oxidation and anti-apoptosis properties.
    J Pharm Biomed Anal. 2013 Jul-Aug;81-82:178-86.
    Identification of senkyunolide I metabolites in rats using ultra performance liquid chromatography/quadrupole-time-of-flight tandem mass spectrometry.[Pubmed: 23666254]
    Ligusticum chuanxiong Hort. (Umbelliferae) has been widely prescribed to treat cardiovascular disease in China for centuries. Senkyunolide I is one of the major bioactive components in L. chuanxiong, which shows pharmacological activities against migraines and oxidative damage.
    In this paper, ultra performance liquid chromatography/quadrupole-time-of-flight tandem mass spectrometry (UPLC/Q-TOF-MS) was applied for the rapid analysis of Senkyunolide I metabolites in rats after its intravenous administration. The non-metabolized parent compound and eighteen metabolites from drug-treated samples in rat plasma, urine and bile were identified. Our analysis indicated that methylation, hydration, epoxidation, glucuronidation and glutathione conjugation were the major pathways of Senkyunolide I metabolism in vivo.
    This study provides important information regarding the metabolism of Senkyunolide I, which will be helpful for understanding its mechanism of action. Furthermore, this work demonstrates the potential of using UPLC/Q-TOF-MS for the rapid and reliable characterization of the metabolites of natural products.
    Senkyunolide I Description
    Source: The roots of Ligusticum chuanxiong hort
    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 4.4583 mL 22.2916 mL 44.5831 mL 89.1663 mL 111.4579 mL
    5 mM 0.8917 mL 4.4583 mL 8.9166 mL 17.8333 mL 22.2916 mL
    10 mM 0.4458 mL 2.2292 mL 4.4583 mL 8.9166 mL 11.1458 mL
    50 mM 0.0892 mL 0.4458 mL 0.8917 mL 1.7833 mL 2.2292 mL
    100 mM 0.0446 mL 0.2229 mL 0.4458 mL 0.8917 mL 1.1146 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.
    Animal Research:
    J Pharm Pharmacol. 2011 Feb;63(2):261-6.
    Effect and mechanism of senkyunolide I as an anti-migraine compound from Ligusticum chuanxiong.[Pubmed: 21235591 ]
    To evaluate the analgesic and anti-migraine activities of Senkyunolide I from Ligusticum chuanxiong.
    Mice were orally administered various doses of Senkyunolide I, and their pain levels were assessed in a hot-plate test and by application of acetic acid. The levels of 5-hydroxytryptamine (5-HT), 5-hydroxytryptophan (5-HTP), 5-hydroxyindoleacetic acid (5-HIAA), norepinephrine (NE) and dopamine (DA) in plasma and brain were assessed, and the monoamine turnover rates (5-HT/5-HTP, 5-HIAA/5-HT and NE/DA) were also calculated. Mice given Senkyunolide I at 16 and 32 mg/kg had significantly elevated pain thresholds in the hot-plate test, and a dose of 32 mg/kg also reduced the number of abdominal writhing responses caused by acetic acid. Significant improvements were observed in the neurotransmitter levels of the drug-treated rats compared with the saline-administered controls. Compared to the rats with nitroglycerin-induced migraines, the levels of nitric oxide in the plasma and whole brain of rats given Senkyunolide I were lower.
    The present study suggests that Senkyunolide I may be an active component of L. chuanxiong, traditionally used to treat migraine. The mechanism of pain relief in migraine model rats may be through adjusting the levels of monoamine neurotransmitters and their turnover rates, as well as decreasing nitric oxide levels in the blood and brain. Therefore, Senkyunolide I may be developed as a potential treatment for migraine pain.