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    CAS No. 116122-36-2 Price
    Catalog No.CFN90315Purity>=98%
    Molecular Weight462.36Type of CompoundFlavonoids
    FormulaC21H18O12Physical DescriptionYellow powder
    Download     COA    MSDSSimilar structuralComparison
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  • Biological Activity
    Description: Breviscapine can reduce the inflammatory response, protect the lungs from inflammatory cascade responses by inhibiting the expression of IL-18 and ICAM-1. Breviscapine inhibits the increased levels of 4-HNE and 8-OHdG, and enhances the antioxidant capacity of cortex tissue. Breviscapine can treat coronary disease, breviscapine injection significantly ameliorates neurologic deficit, reduces infarct volume and water content, and suppresses the levels of NSE in a time-dependent manner, may the mechanism is by up-regulating the expression of Nrf2/HO-1 pathway .
    Targets: ROCK | NOS | PDE | Nrf2 | HO-1 | IL Receptor
    In vivo:
    J Sex Med. 2014 Sep;11(9):2143-52.
    Icariin combined with breviscapine improves the erectile function of spontaneously hypertensive rats.[Pubmed: 24912989]
    The impaired erectile response in spontaneously hypertensive rats (SHR) is caused by increased signaling of RhoA/Rho-kinase and decreased signaling of nitric oxide (NO). Icariin improves erectile function via upregulating multitargets in NO/cyclic guanosine monophosphate (NO/cGMP) pathway, which Breviscapine accomplishes by downregulating RhoA/Rho-kinase pathway. To investigate the effect and mechanism of icariin combined with Breviscapine on the erectile function of SHR.
    Five 12-week-old male Wistar-Kyoto (WKY) rats and 20 age-matched male SHR were evenly randomized into WKY rats control group, SHR control group, icariin-treated group, Breviscapine-treated group, and combined treatment group treated by vehicle, icariin, Breviscapine, and icariin plus Breviscapine, respectively, by gavage for four successive weeks. Maximum intracavernosal pressure/mean arterial pressure (ICPmax/MAP) and the expression of endothelial nitric oxide synthase (eNOS), neuronal nitric oxide synthase (nNOS), phosphodiesterase type 5 inhibitors (PDE5), and Rho-associated, coiled-coil containing protein kinase 1 and 2 (ROCK1 and ROCK2) in the cavernous tissues were determined. The ICPmax/MAP in the combined treatment group was significantly increased compared with SHR control group, icariin-treated group, and Breviscapine-treated group. The expression of eNOS and nNOS was significantly higher in the combined treatment group than in SHR control group, icariin-treated group, and Breviscapine-treated group (P < 0.05). The expression of PDE5 was significantly lower in the icariin-treated group than in SHR control group (P < 0.05). The expression of ROCK1 was significantly lower in the combined treatment group than in other groups (P < 0.05). The expression of ROCK2 was significantly higher in SHR control group than in WKY rats control group, icariin-treated group, and combined treatment group (P < 0.05). Among these groups, the expression of eNOS and nNOS was the strongest, and ROCK1 was the lowest in WKY rats control group.
    Icariin combined with Breviscapine has synergistic effects on erectile function of SHR through different signal pathways.
    J Pharm Pharmacol. 2014 Jul;66(7):903-11.
    Improved oral bioavailability of breviscapine via a Pluronic P85-modified liposomal delivery system.[Pubmed: 24697705]
    Breviscapine, a hydrophobic drug used for treating cardiovascular disease, was encapsulated in liposomes to improve its pharmaceutical characteristics. This study describes a novel liposome composition approach to specifically inhibit the P-glycoprotein efflux system.
    Breviscapine-loaded Pluronic P85-coated liposomes were prepared by the thin film hydration technique. The particle size, zeta potential and encapsulation efficiency of the formulations were characterized. In-vitro drug release and permeability of Caco-2 cells were investigated. In-vitro characteristics and pharmacokinetics of the liposomes were evaluated in rat studies. The Pluronic P85-modified liposomes dispersed individually and had an approximate diameter of 118.8 ± 4.9 nm and a zeta potential of -35.4 ± 1.5 mV. Encapsulation efficiency was more than 90%. The use of the P85-coated liposomes resulted in significantly (P<0.05) increased absorption of Breviscapine in Caco-2 cells and in 5.6-fold enhancement in its oral bioavailability in rats.
    The P85-modified liposomes for the oral delivery of Breviscapine were prepared using l-α-phosphatidylcholine (soy-hydrogenated) and cholesterol with a narrow size distribution. This method seems to effectively enhance the bioavailability of Breviscapine in rats.
    PLoS One. 2015 Jun 8;10(6):e0129969.
    Breviscapine Injection Improves the Therapeutic Effect of Western Medicine on Angina Pectoris Patients.[Pubmed: 26052709]
    To evaluate the beneficial and adverse effects of Breviscapine injection in combination with Western medicine on the treatment of patients with angina pectoris.
    The Cochrane Central Register of Controlled Trials, Medline, Science Citation Index, EMBASE, the China National Knowledge Infrastructure, the Wanfang Database, the Chongqing VIP Information Database and the China Biomedical Database were searched to identify randomized clinical trials (RCTs) that evaluated the effects of Western medicine compared to Breviscapine injection plus Western medicine on angina pectoris patients. The included studies were analyzed using RevMan 5.1.0 software. The literature search yielded 460 studies, wherein 16 studies matched the selection criteria. The results showed that combined therapy using Breviscapine plus Western medicine was superior to Western medicine alone for improving angina pectoris symptoms (OR =3.77, 95% Cl: 2.76~5.15) and also resulted in increased electrocardiogram (ECG) improvement (OR=2.77, 95% Cl: 2.16~3.53).
    The current evidence suggests that Breviscapine plus Western medicine achieved a superior therapeutic effect compared to Western medicine alone.
    Breviscapine Description
    Source: The herbs of Erigeron breviscapus
    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.

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    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 2.1628 mL 10.8141 mL 21.6282 mL 43.2563 mL 54.0704 mL
    5 mM 0.4326 mL 2.1628 mL 4.3256 mL 8.6513 mL 10.8141 mL
    10 mM 0.2163 mL 1.0814 mL 2.1628 mL 4.3256 mL 5.407 mL
    50 mM 0.0433 mL 0.2163 mL 0.4326 mL 0.8651 mL 1.0814 mL
    100 mM 0.0216 mL 0.1081 mL 0.2163 mL 0.4326 mL 0.5407 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 Ethnopharmacol. 2014;151(1):660-6.
    Therapeutic time window and underlying therapeutic mechanism of breviscapine injection against cerebral ischemia/reperfusion injury in rats.[Pubmed: 24291152]
    Breviscapine injection is a Chinese herbal medicine standardized product extracted from Erigeron breviscapus (Vant.) Hand.-Mazz. It has been widely used for treating cardiovascular and cerebrovascular diseases. However, the therapeutic time window and the action mechanism of Breviscapine are still unclear. The present study was designed to investigate the therapeutic time window and underlying therapeutic mechanism of Breviscapine injection against cerebral ischemic/reperfusion injury.
    Sprague-Dawley rats were subjected to middle cerebral artery occlusion for 2h followed by 24h of reperfusion. Experiment part 1 was used to investigate the therapeutic time window of Breviscapine. Rats were injected intravenously with 50mg/kg Breviscapine at different time-points of reperfusion. After 24h of reperfusion, neurologic score, infarct volume, brain water content and serum level of neuron specific enolase (NSE) were measured in a masked fashion. Part 2 was used to explore the therapeutic mechanism of Breviscapine. 4-Hydroxy-2-nonenal (4-HNE), 8-hydroxyl-2'- deoxyguanosine (8-OHdG) and the antioxidant capacity of ischemia cortex were measured by ELISA and ferric-reducing antioxidant power (FRAP) assay, respectively. Immunofluorescence and western blot analysis were used to analyze the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1). Part 1: Breviscapine injection significantly ameliorated neurologic deficit, reduced infarct volume and water content, and suppressed the levels of NSE in a time-dependent manner. Part 2: Breviscapine inhibited the increased levels of 4-HNE and 8-OHdG, and enhanced the antioxidant capacity of cortex tissue. Moreover, Breviscapine obviously raised the expression of Nrf2 and HO-1 proteins after 24h of reperfusion.
    The therapeutic time window of Breviscapine injection for cerebral ischemia/reperfusion injury seemed to be within 5h after reperfusion. By up-regulating the expression of Nrf2/HO-1 pathway might be involved in the therapeutic mechanism of Breviscapine injection.
    Exp Ther Med. 2013 Nov;6(5):1322-1326.
    Breviscapine reduces acute lung injury induced by left heart ischemic reperfusion in rats by inhibiting the expression of ICAM-1 and IL-18.[Pubmed: 24223666]
    It has been demonstrated that Breviscapine is able to treat coronary disease and reduce the inflammatory response; however, there are no relevant reports concerning its effects on the expression of inflammatory factors in acute lung injury induced by left heart ischemic reperfusion and the underlying mechanisms.
    In this study, we created a left heart ischemia-reperfusion model in rats to investigate the effects of Breviscapine on the expression of interleukin 18 (IL-18) and intercellular adhesion molecule-1 (ICAM-1), as well as to determine the possible mechanisms involved in the protective effects of Breviscapine on respiratory function. The left heart ischemia-reperfusion model was created by ligating the anterior descending branch of the coronary artery for 30 mins followed by reperfusion. Rats in the treatment group (TG) were treated with Breviscapine (10 mg/kg) and the rats in the control group (CG) received normal saline. Ten rats in the two groups were sacrificed at three points: 30 min after ligating (T1), 30 min after reperfusion (T2) and 60 min after reperfusion (T3). A respiration curve was produced and the arterial partial pressure of oxygen (PaO2) was measured for all rats. Additionally, the expression levels of IL-18 and ICAM-1 were determined and the correlation between IL-18 and ICAM-1 expression in lung tissue was analyzed. The level of IL-18 in peripheral blood and bronchialalveolar lavage fluid (BALF) was also measured. The respiration amplitude was lower and the duration time was shorter in the TG rats than in the CG rats at T1, T2 and T3. The expression levels of IL-18 and ICAM-1 in the TG group were clearly reduced. The level of IL-18 in the peripheral blood and BALF was downregulated following the administration of Breviscapine.
    These results demonstrate that Breviscapine inhibits the expression of IL-18 and ICAM-1, thereby protecting the lungs from inflammatory cascade responses.