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Praeruptorin A
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Product Name Praeruptorin A
Price: $60 / 20mg
CAS No.: 73069-25-7
Catalog No.: CFN98139
Molecular Formula: C21H22O7
Molecular Weight: 386.40 g/mol
Purity: >=98%
Type of Compound: Coumarins
Physical Desc.: Powder
Source: The roots of Peucedanum praeruptorum Dunn.
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Download: COA    MSDS    SDF    Manual
Similar structural: Comparison (Web)  (SDF)
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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 / $10.8 / In-stock
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Related Screening Libraries
Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
10 mM * 1 mL in DMSO / Inquiry / In-stock
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Biological Activity
Description: Praeruptorin A exerts neuroprotective, anti-osteoclastogenic, anti-inflammatory, distinct relaxant effects, it is beneficial to facilitate nestin expression in myocarditis,and suitable in treatment of early myocarditis. Praeruptorin A can significantly up-regulate UGT1A1 expression in HepG2 cells partially via the CAR-mediated pathway. Praeruptorin A inhibited p38/Akt-c-Fos-NFATc1 signaling and PLCγ-independent Ca2+ oscillation.
Targets: Calcium Channel | p38MAPK | Akt | NO | IL Receptor | TNF-α | NF-kB | IkB | Bcl-2/Bax | SOD | IKK
In vitro:
J Nat Prod. 2015 Apr 24;78(4):776-82.
Praeruptorin a inhibits in vitro migration of preosteoclasts and in vivo bone erosion, possibly due to its potential to target calmodulin.[Pubmed: 25734761]
Excessive activity and/or increased number of osteoclasts lead to bone resorption-related disorders. Here, we investigated the potential of Praeruptorin A to inhibit migration/fusion of preosteoclasts in vitro and bone erosion in vivo.
METHODS AND RESULTS:
Praeruptorin A inhibited the RANKL-induced migration/fusion of preosteoclasts accompanied by the nuclear translocation of NFATc1, a master regulator of osteoclast differentiation. Antimigration/fusion activity of Praeruptorin A was also confirmed by evaluating the mRNA expression of fusion-mediating molecules. In silico binding studies and several biochemical assays further revealed the potential of Praeruptorin A to bind with Ca(2+)/calmodulin and inhibit its downstream signaling pathways, including the Ca(2+)/calmodulin-CaMKIV-CREB and Ca(2+)/calmodulin-calcineurin signaling axis responsible for controlling NFATc1. In vivo application of Praeruptorin A significantly reduced lipopolysaccharide-induced bone erosion, indicating its possible use to treat bone resorption-related disorders.
CONCLUSIONS:
In conclusion, Praeruptorin A has the potential to inhibit migration/fusion of preosteoclasts in vitro and bone erosion in vivo by targeting calmodulin and inhibiting the Ca(2+)/calmodulin-CaMKIV-CREB-NFATc1 and/or Ca(2+)/calmodulin-calcineurin-NFATc1 signaling axis.
PLoS One. 2014 Feb 21;9(2):e88974.
Anti-osteoclastogenic activity of praeruptorin A via inhibition of p38/Akt-c-Fos-NFATc1 signaling and PLCγ-independent Ca2+ oscillation.[Pubmed: 24586466]
A decrease of bone mass is a major risk factor for fracture. Several natural products have traditionally been used as herbal medicines to prevent and/or treat bone disorders including osteoporosis. Praeruptorin A is isolated from the dry root extract of Peucedanum praeruptorum Dunn and has several biological activities, but its anti-osteoporotic activity has not been studied yet.
METHODS AND RESULTS:
The effect of Praeruptorin A on the differentiation of bone marrow-derived macrophages into osteoclasts was examined by phenotype assay and confirmed by real-time PCR and immunoblotting. The involvement of NFATc1 in the anti-osteoclastogenic action of Praeruptorin A was evaluated by its lentiviral ectopic expression. Intracellular Ca(2+) levels were also measured. Praeruptorin A inhibited the RANKL-stimulated osteoclast differentiation accompanied by inhibition of p38 and Akt signaling, which could be the reason for Praeruptorin A-downregulated expression levels of c-Fos and NFATc1, transcription factors that regulate osteoclast-specific genes, as well as osteoclast fusion-related molecules. The anti-osteoclastogenic effect of Praeruptorin A was rescued by overexpression of NFATc1. Praeruptorin A strongly prevented the RANKL-induced Ca(2+) oscillation without any changes in the phosphorylation of PLCγ.
CONCLUSIONS:
Praeruptorin A could exhibit its anti-osteoclastogenic activity by inhibiting p38/Akt-c-Fos-NFATc1 signaling and PLCγ-independent Ca(2+) oscillation.
Phytother Res. 2011 Apr;25(4):550-6.
Praeruptorin A inhibits lipopolysaccharide-induced inflammatory response in murine macrophages through inhibition of NF-κB pathway activation.[Pubmed: 20842678 ]
Praeruptorin A (PA) is a pyranocoumarin compound isolated from the dried root of Peucedanum praeruptorum Dunn (Umbelliferae). However, the antiinflammatory effect of PA has not been reported.
METHODS AND RESULTS:
The present study investigated the antiinflammatory effect of PA in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. PA significantly inhibited the LPS-induced production of nitric oxide (NO), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). The mRNA and protein expressions of inducible nitric oxide synthase (iNOS), IL-1β and TNF-α were also suppressed by this compound. Further study showed that PA decreased the cytoplasmic loss of inhibitor κB-α (IκB-α) protein and inhibited the translocation of NF-κB from cytoplasm to nucleus.
CONCLUSIONS:
Taken together, the results suggest that PA may exert antiinflammatory effects in vitro in LPS-stimulated RAW 264.7 macrophages through inhibition of NF-κB signal pathway activation.
In vivo:
Pharmacology & Clinics of Chinese Materia Medica, 2007, 23(3):21-3.
Praeruptorin A upregulates expression of nestin in experimental autoimmune myocarditis of rats[Reference: WebLink]
To investigate the influence of dl-Praeruptorin A(Pd-Ia) on expression of intermediate filament protein nestin and its cardioprotective actions in myocarditis.[WT5"HZ]
METHODS AND RESULTS:
Effect of Pd-Ia on expression of nestin was evaluated in rats that had recovered from experimental autoimmune myocarditis(EAM).Wistar rats were divided into 5 groups,including group sham,group natural saline,group solvent control(polyethylene glycol),group Pd-Ia 1.0 mg/kg,and group positive control(verapamil0.5 mg/kg),respectively.Thereafter,all animals were immunized with pig cardiac myosin on day 0.Drugs were administered twice through abdominal cavity on day 20 and day 21,respectively.Four hours after second administration,rats are executed.Expression of nestin in myocardium was detected by Western blot analysis.Heart weight/body weight ratio,myocardial enzyme spectrum,and histopathology were measured simultaneously. Results:Pd-Ia upregulated expression of nestin and relieved myocardial injury in EAM of rats.Values of relative optic density in Pd-Ia(1.0 mg/kg) group were increased from 37.5 ± 3 to 61 ± 4(P0.05,vs solvent,n=5).
CONCLUSIONS:
[WT5"BZ] Pd-Ia was beneficial to facilitate nestin expression in myocarditis,and suitable in treatment of early myocarditis.
Praeruptorin A Description
Source: The roots of Peucedanum praeruptorum Dunn.
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.

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 2.588 mL 12.94 mL 25.8799 mL 51.7598 mL 64.6998 mL
5 mM 0.5176 mL 2.588 mL 5.176 mL 10.352 mL 12.94 mL
10 mM 0.2588 mL 1.294 mL 2.588 mL 5.176 mL 6.47 mL
50 mM 0.0518 mL 0.2588 mL 0.5176 mL 1.0352 mL 1.294 mL
100 mM 0.0259 mL 0.1294 mL 0.2588 mL 0.5176 mL 0.647 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
Cell Research:
Yao Xue Xue Bao. 2013 May;48(5):794-8.
Induction of UGT1A1 expression by praeruptorin A and praeruptorin C through hCAR pathway.[Pubmed: 23888707]
This study is purposed to investigate the effects of Praeruptorin A (PA) and praeruptorin C (PC) on UGT1A1 in HepG2 cells through hCAR pathway.
METHODS AND RESULTS:
PA and PC were incubated with HepG2 cells for 24 h and 48 h, mRNA and protein expressions of UGT1A1 were determined by real-time PCR and Western blotting assays. Additionally, effects of PA and PC on UGT1A1 mRNA and protein expressions were also measured after transient transfection of a specific CAR siRNA for 72 h in HepG2 cells. UGT1A1 mRNA and protein expression levels were significantly increased by PA and PC after incubation for 48 h. Moreover, the mRNA and protein up-regulations of UGT1A1 were attenuated by transient transfection of a specific CAR siRNA, suggesting the induction was mediated by CAR.
CONCLUSIONS:
The results suggest that PA and PC can significantly up-regulate UGT1A1 expression partially via the CAR-mediated pathway.
Chem Biol Interact. 2010 Jul 30;186(2):239-46.
(+/-)-Praeruptorin A enantiomers exert distinct relaxant effects on isolated rat aorta rings dependent on endothelium and nitric oxide synthesis.[Pubmed: 20433815 ]
Praeruptorin A (PA) is a pyranocoumarin compound isolated from the dried root of Peucedanum praeruptorum Dunn (Umbelliferae). However, the antiinflammatory effect of PA has not been reported. The present study investigated the antiinflammatory effect of PA in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells.
METHODS AND RESULTS:
PA significantly inhibited the LPS-induced production of nitric oxide (NO), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). The mRNA and protein expressions of inducible nitric oxide synthase (iNOS), IL-1β and TNF-α were also suppressed by this compound. Further study showed that PA decreased the cytoplasmic loss of inhibitor κB-α (IκB-α) protein and inhibited the translocation of NF-κB from cytoplasm to nucleus.
CONCLUSIONS:
Taken together, the results suggest that PA may exert antiinflammatory effects in vitro in LPS-stimulated RAW 264.7 macrophages through inhibition of NF-κB signal pathway activation.
Animal Research:
Acta Pharmacol Sin. 2002 Sep;23(9):769-74.
Effects of dl-praeruptorin A on interleukin-6 level and Fas, bax, bcl-2 protein expression in ischemia-reperfusion myocardium.[Pubmed: 12230942]
To investigate the effects of dl-praeruptorin (Pd-Ia) on interleukin-6 (IL-6) level and apoptosis-related protein expression in ischemia-reperfusion myocardium.
METHODS AND RESULTS:
Left anterior descending coronary artery was subjected to 30 min ischemia followed by 120 min reperfusion in open-chest anesthetized rats. Serum IL-6 level was measured by radioimmunoassay. Apoptosis-related protein Fas, bax, and bcl-2 expression was detected by immunohistochemistry and computer image analysis system. Infiltration of neutrophils was observed using Hematoxylin-Eosin staining under optical microscope. Pd-Ia 2.0 mg/kg iv lowered serum IL-6 level and Fas, bax, bcl-2 expression under conditions with hypotension and without changes on heart rate, but increased the ratio of bcl-2/bax. There existed a close linearity and positive correlation between IL-6 level and Fas, bax, bcl-2 expression. Whereas, the infiltration of neutrophils was mild.
CONCLUSIONS:
Pd-Ia elicits a novel target in the therapeutic prevention of postischemic cardiomyocyte death. The reason might be associated with modulating the expression of some immediate-early genes including IL-6, Fas, bax, and bcl-2 in ischemia-reperfusion myocardium.
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