Praeruptorin E

Praeruptorin E
Product Name Praeruptorin E
CAS No.: 78478-28-1
Catalog No.: CFN90449
Molecular Formula: C24H28O7
Molecular Weight: 428.47 g/mol
Purity: >=98%
Type of Compound: Coumarins
Physical Desc.: Powder
Targets: TNF-α | IL Receptor | NF-kB | p65 | IkB | IKK
Source: The roots of Peucedanum praeruptorum Dunn.
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Price:
Praeruptorin E is a cardiotonic agent with selective cardiac calcium channel agonistic effect, it can relax swine coronary artery and decrease contractility in guinea-pig left atria. Praeruptorin E may be useful in the therapy of lung injury, it can protect mice from hydrochloric acid (HCl)-induced lung injury by inhibiting polymorphonuclear leukocytes (PMNs) influx, IL-6 release and protein exudation.
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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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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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    Eur. J. Pharmacol., 2013, 710(1-3):39-48.
    Praeruptorin E and D attenuate lipopolysaccharide/hydrochloric acid induced acute lung injury in mice.[Pubmed: 23588118]
    Acute lung injury is a life-threatening syndrome characterized by overwhelming lung inflammation and increased microvascular permeability, which causes a high mortality rate worldwide. The dry root of Peucedanum praeruptorum Dunn has been long used to treat respiratory diseases in China. In the present study, Praeruptorin E, D, C and A (PE, PD, PC and PA), four pyranocoumarins extracted from this herb, have been investigated for the pharmacological effects in experimental lung injury mouse models.
    METHODS AND RESULTS:
    In lipopolysaccharide (LPS) challenged mice, PA and PC did not show protective effect against lung injury at the dose of 80 mg/kg. However, PD and PE significantly inhibited the infiltration of activated polymorphonuclear leukocytes (PMNs) and decreased the levels of TNF-α and IL-6 in bronchoalveolar lavage fluid at the same dose. There was no statistically significant difference between PD and PE group. Further study demonstrated that PD and PE suppressed protein extravasations in bronchoalveolar lavage fluid, attenuated myeloperoxidase (MPO) activity and the pathological changes in the lung. Both PD and PE suppressed LPS induced Nuclear Factor-kappa B (NF-κB) pathway activation in the lung by decreasing the cytoplasmic loss of Inhibitor κB-α (IκB-α) protein and inhibiting the translocation of p65 from cytoplasm to nucleus. We also extended our study to acid-induced acute lung injury and found that these two compounds protected mice from hydrochloric acid (HCl)-induced lung injury by inhibiting PMNs influx, IL-6 release and protein exudation.
    CONCLUSIONS:
    Taken together, these results suggested that PD and PE might be useful in the therapy of lung injury.
    Eur. J. Pharmacol. 1988, 155(3):293-6.
    Effects of praeruptorin C and E isolated from 'Qian-Hu' on swine coronary artery and guinea-pig atria.[Pubmed: 3234487]

    METHODS AND RESULTS:
    Praeruptorin C and Praeruptorinn E isolated from Peucedanum praeruptorum Dunn. decreased the maximum contractile effect of Ca2+ in potassium-depolarized swine coronary strips and shifted the concentration-response curve to the right in a non-parallel manner. The calcium antagonistic activity of praeruptorin C and E expressed as pD'2 value was 5.7 and 5.2, respectively. Nifedipine, with a pD'2 value of 6.88, was used as a known calcium antagonistic drug to compare the potency of the drugs studied. The relaxation induced by praeruptorin C was concentration-dependent and the IC50 value was 79 microM. Praeruptorin C also reduced the maximum contractile response and shifted the concentration-response curve for calcium to the right in a non-parallel manner in potassium-depolarized guinea-pig left atria (pD'2 = 5.52) but its potency was much less than that of nifedipine (pD'2 = 7.19).
    CONCLUSIONS:
    The results suggest that praeruptorin C and Praeruptorin E relaxed swine coronary artery and decreased contractility in guinea-pig left atria. These effects are similar in many respects to those displayed by drugs that have calcium entry blocking activity.
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