|Source:||The roots of Polygala tenuifolia Willd.|
|Biological Activity or Inhibitors:||1. Euxanthone-induced neurite outgrowth was actively regulated by transcription factor E2F-5 via PKC pathway.
2. Euxanthone induces its vasodilator effect through inhibition of calcium-sensitive mechanisms activated by protein kinase C.
3. Euxanthone has vasorelaxation effect, may be through multiple pathways involved PKC-mediated signal pathway and calcium-independent pathway.
4. Euxanthone-induced differentiation of the neuroblastoma BU-1 cells may be mediated through the differential expression of PKC-alpha, -beta, -delta, -lambda and -zeta isoforms.
|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: firstname.lastname@example.org
|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.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||4.3821 mL||21.9106 mL||43.8212 mL||87.6424 mL||109.553 mL|
|5 mM||0.8764 mL||4.3821 mL||8.7642 mL||17.5285 mL||21.9106 mL|
|10 mM||0.4382 mL||2.1911 mL||4.3821 mL||8.7642 mL||10.9553 mL|
|50 mM||0.0876 mL||0.4382 mL||0.8764 mL||1.7528 mL||2.1911 mL|
|100 mM||0.0438 mL||0.2191 mL||0.4382 mL||0.8764 mL||1.0955 mL|
Phytomedicine. 2010 Jul;17(8-9):690-2.
|Mechanism of the vasodilator effect of Euxanthone in rat small mesenteric arteries.[Pubmed: 20097048]|
|In the present work we investigated the mechanism involved in the vasodilator effect induced by Euxanthone in rat small mesenteric arteries. We observed that Euxanthone induced concentration-dependent vasodilatation in arteries by a mechanism independent on the release of endothelial factors, such as nitric oxide (NO) and cyclooxygenase-derived factors. In addition our results also suggest that Euxanthone induced its vasodilator effect through inhibition of calcium-sensitive mechanisms activated by protein kinase C, rather than by inhibition of contractions dependent on the release of the intracellular calcium stores or by inhibition of voltage-operated calcium channels.|
Vascul Pharmacol. 2006 Aug;45(2):96-101.
|Vasorelaxant effect of euxanthone in the rat thoracic aorta.[Pubmed: 16678494]|
|This study was undertaken to investigate the effect of Euxanthone on isolated rat thoracic aorta. Euxanthone concentration-dependently relaxed high K+-induced sustained contractions with IC50 values of 32.28+/-1.73 microM and this inhibition was antagonized by increasing the Ca2+ concentration in the medium. These results indicated that Euxanthone may have calcium antagonistic property. Euxanthone also relaxed norepinephrine (NE)-induced sustained contractions with IC50 values of 32.50+/-2.15 microM and this relaxant effect was unaffected by the removal of endothelium or by the presence of propranolol, indomethacin, glibenclamide or N(omega)-nitro-L-arginine. Moreover, Euxanthone inhibited both the phasic and tonic contractions induced by NE in a concentration-dependent manner and showed more potent inhibition on phasic contraction (P < 0.01). Pre-treatment with Euxanthone inhibited vascular contraction induced by phorbol 12, 13-dibutyrate (PDBu), a protein kinase C (PKC) agonist, in either the presence or absence of Ca2+ in the solution with IC50 values of 20.15+/-1.56 and 18.30+/-1.62 microM, respectively. However, when the tissues were treated with Euxanthone after the PDBu-induced contraction had reached a steady state, the tension was not affected by Euxanthone. This study also showed that the inhibitory effect of pre-treatment of Euxanthone was more potent than the post-treatment after the tension had reached a steady state. These results suggested that the vasorelaxation of Euxanthone may be through multiple pathways involved PKC-mediated signal pathway and calcium-independent pathway besides the direct inhibition of calcium influx and its vasorelaxant effect is more active on calcium-independent pathway and more sensitive to the initial stage of contraction.|
Planta Med. 2001 Jul;67(5):400-5.
|Expression of protein kinase C isoforms in euxanthone-induced differentiation of neuroblastoma cells.[Pubmed: 11488451]|
|Euxanthone, a potent neuritogenic compound isolated from the roots of the medicinal herb Polygala caudata, has recently been shown to induce the differentiation of murine neuroblastoma Neuro 2A (BU-1) cells. In this study, the role of protein kinase C (PKC) and the expression of various PKC isoforms in Euxanthone-treated BU-1 cells were examined. mRNA phenotyping using the reverse-transcription polymerase chain reaction (RT-PCR) showed that BU-1 cells express six different PKC isoforms, namely PKC-alpha, -beta, -delta, -epsilon, -lambda, and -zeta. Differential regulation and expression of PKC isoforms was observed in BU-1 cells treated with 100 microM Euxanthone. PKC-apha, -beta, -delta, -lambda and -zeta were all up-regulated, with 1.7- to 9.5-fold increase, at around 30 to 60 minutes after Euxanthone treatment. The expression level of PKC-epsilon remained relatively constant during the treatment. PKC-gamma, -eta, and -theta were not detected in both untreated and Euxanthone-treated BU-1 cells. Staurosporine, a broad spectrum PKC inhibitor, was found to inhibit both spontaneous and Euxanthone-induced neuritogenesis in BU-1 cells. A significant reduction of the Euxanthone-induced neuritogenic effect was also observed when the PKC isoform-specific inhibitor Go6976 was included in the culture. These results suggest that the Euxanthone-induced differentiation of the neuroblastoma BU-1 cells may be mediated through the differential expression of PKC-alpha, -beta, -delta, -lambda and -zeta isoforms.|
Int J Biochem Cell Biol. 2006;38(8):1393-401.
|Involvement of protein kinase C and E2F-5 in euxanthone-induced neurite differentiation of neuroblastoma.[Pubmed: 16546434]|
|Euxanthone, a neuritogenic agent isolated from the medicinal herb Polygala caudata, has been shown to induce morphological differentiation and neurite outgrowth in murine neuroblastoma Neuro 2a cells (BU-1 subclone). In order to elucidate the underlying mechanisms of Euxanthone-induced neurite outgrowth, a proteomic approach was employed. In the present study, two dimensional (2-D) gel electrophoresis and matrix-assisted laser desorption/ionization-time of flight (MALDI-ToF) mass spectrometry were performed to investigate the alterations in protein expression profile of Euxanthone-treated BU-1 cells. Fourteen identified proteins were changed in expression levels after induction of neurite growth. These proteins included participants in transcription and cell cycle regulation, calcium influx and calcium signaling, fatty acid metabolism, cytoskeleton reorganization, casein kinase signal transduction, putative transbilayer amphipath transport and protein biosynthesis. Among the 14 identified proteins, E2F transcription factor 5 (E2F-5) was significantly up-regulated after Euxanthone treatment. Go6976, a protein kinase C (PKC) alpha/betaI inhibitor, was found to inhibit neuritogenesis and expression of E2F-5 in the Euxanthone-treated BU-1 cells, while SH-6, the Akt/PKB inhibitor, had no inhibitory effect. The gene silencing of E2F-5 by small interfering RNA (siRNA) was found to abolish the Euxanthone-induced neurite outgrowth. In conclusion, these results indicated that the transcription factor E2F-5 was actively involved in the regulation of Euxanthone-induced neurite outgrowth via PKC pathway.|
Planta Med. 2002 Nov;68(11):1039-41.
|Differential activation of protein kinase C isoforms by euxanthone, revealed by an in vivo yeast phenotypic assay.[Pubmed: 12451499]|
|The protein kinase C (PKC) modulatory effects of Euxanthone, isolated from the wood of Cratoxylum maingayi, on isoforms alpha, betaI, delta, eta and zeta were characterised using an alternative in vivo yeast phenotypic assay. The present study shows that Euxanthone can activate isoforms alpha, betaI, delta, eta and zeta, being more effective on PKC-betaI, -delta, -eta and -zeta than the established PKC activators used (the phorbol ester PMA and arachidonic acid for PKC-zeta). Furthermore, Euxanthone presents differences on its potency towards individual PKC isoforms, showing a remarkable selectivity for PKC-zeta. These results can help to clarify the molecular basis of the Euxanthone-mediated effects.|