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More articles cited ChemFaces products.
Korean J. of Food Sci. and TechApril 2016Sci Rep. 2016 Apr 27Molecules.2013 Jun 24;18(7):7376-88.J Ethnopharmacol. 2016 Jul 12.Journal of Analytical ChemistryAug. 2017;
Evidence-Based Comp. & Alter. Med.Dec. 27, 2015J. of Pha. and Biomed. Analysis25 Jan. 2016Am J Chin Med.2016;44(8)PhytomedicineFeb. 11. 2016Sci Rep. 2016; 6: 25094.2016 Apr 27;6:25094.
Am J Chin Med.2016;44(6)J Bone Miner Res. 2017 Jul 26.Fitoterapia. 2018 Jan;Journal of Functional FoodsFeb. 2018;
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||Oxysophocarpine shows anti-inflammatory, neuroprotective,
anticonvulsant, and anti-nociceptive effects, it also attenuates inflammatory pain by suppressing the levels of phosphorylation of extracellular signal-regulated kinase 1/2, cyclooxygenase-2, prostaglandin E2, tumor necrosis factor α, interleukin-1 beta and interleukin-6.
||ERK | COX | PGE | TNF-α | IL Receptor | Caspase | GABA Receptor | Bcl-2/Bax | P450 (e.g. CYP17)|
|Pharm Biol. 2014 Aug;52(8):1052-9. |
|Neuroprotective effects of oxysophocarpine on neonatal rat primary cultured hippocampal neurons injured by oxygen-glucose deprivation and reperfusion.[Pubmed: 24601951]|
| Oxysophocarpine (OSC), a quinolizidine alkaloid extracted from leguminous plants of the genus Robinia, is traditionally used for various diseases including neuronal disorders. This study investigated the protective effects of Oxysophocarpine on neonatal rat primary-cultured hippocampal neurons were injured by oxygen-glucose deprivation and reperfusion (OGD/RP).|
METHODS AND RESULTS:
Cultured hippocampal neurons were exposed to OGD for 2 h followed by a 24 h RP. Oxysophocarpine (1, 2, and 5 μmol/L) and nimodipine (Nim) (12 μmol/L) were added to the culture after OGD but before RP. The cultures of the control group were not exposed to OGD/RP. MTT and LDH assay were used to evaluate the protective effects of Oxysophocarpine. The IC50 of OSC was found to be 100 μmol/L. Treatment with Oxysophocarpine (1, 2, and 5 μmol/L) attenuated neuronal damage (p < 0.001), with evidence of increased cell viability (p < 0.001) and decreased cell morphologic impairment. Furthermore, Oxysophocarpine increased MMP (p < 0.001), but it inhibited [Ca(2+)]i (p < 0.001) elevation in a dose-dependent manner at OGD/RP. Oxysophocarpine (5 μmol/L) also decreased the expression of caspase-3 (p < 0.05) and caspase-12 (p < 0.05).
The results suggested that Oxysophocarpine has significant neuroprotective effects that can be attributed to inhibiting endoplasmic reticulum (ER) stress-induced apoptosis.
|Planta Med. 2015 Jul;81(10):791-7. |
|Oxysophocarpine Ameliorates Carrageenan-induced Inflammatory Pain via Inhibiting Expressions of Prostaglandin E2 and Cytokines in Mice.[Pubmed: 26132856]|
|Oxysophocarpine is an alkaloid extracted from Sophora alopecuroides. |
METHODS AND RESULTS:
Mouse ear swelling tests and carrageenan-induced paw edema tests were used to investigate the effects of Oxysophocarpine on inflammatory pain in mice. Morphological changes on inflamed paw sections were measured by hematoxylin-eosin staining. Oxysophocarpine also significantly reduced the paw edema volume and improved mechanical allodynia threshold value on carrageenan-induced inflammatory pain, as well as relieved paw tissues inflammatory damage and reduced the numbers of neutrophils in mice. Oxysophocarpine significantly suppressed over-expression of cyclooxygenase-2, tumor necrosis factor α, interleukin-1 beta, interleukin-6 and prostaglandin E2, and inhibited the over-phosphorylation of extracellular signal-regulated kinase 1/2.
Based on these findings we propose that Oxysophocarpine attenuates inflammatory pain by suppressing the levels of phosphorylation of extracellular signal-regulated kinase 1/2, cyclooxygenase-2, prostaglandin E2, tumor necrosis factor α, interleukin-1 beta and interleukin-6.
|Mol Med Rep. 2013 Jun;7(6):1819-25. |
|Oxysophocarpine induces anti-nociception and increases the expression of GABAAα1 receptors in mice.[Pubmed: 23563643]|
|Oxysophocarpine (OSC) is an alkaloid extracted from Siphocampylus verticillatus. The aim of this study was to investigate the anti-nociceptive effects of Oxysophocarpine through systemic and intracerebroventricular administration in mice. Moreover, to evaluate its effectiveness and mechanism of action, this study investigated whether Oxysophocarpine altered the expression of γ-aminobutyric acid type A α1 (GABAAα1) receptors in the central nervous system.
METHODS AND RESULTS:
Thermal and chemical behavioral models of nociception were used to assess the anti‑nociceptive action of Oxysophocarpine.Oxysophocarpine was administered intraperitoneally (i.p.) or intracerebroventricularly (i.c.v.). Results showed that Oxysophocarpine (80 mg/kg, i.p.) significantly increased the tail withdrawal threshold with a peak effect of 25.46% maximal possible effect (MPE) at 60 min (P﹤0.01). Additionally, Oxysophocarpine (80 mg/kg) increased the positive staining of GABAAα1 receptors in cells.
In conclusion, Oxysophocarpine administration is suggested to have anti-nociceptive effects on the central and peripheral nervous systems. The involvement of GABAA receptors in the anti-nociceptive activity of Oxysophocarpine is currently being investigated.
||The roots of Styphnolobium japonicum (L.) Schott.
||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
||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
||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.
Recent ChemFaces New Products and Compounds
Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals
Cell. 2018 Jan 11;172(1-2):249-261.e12. doi: 10.1016/j.cell.2017.12.019.PMID: 29328914
Mol Cell. 2017 Nov 16;68(4):673-685.e6. doi: 10.1016/j.molcel.2017.10.022.PMID: 29149595
Scientific Reports 2017 Dec 11;7(1):17332.doi: 10.1038/s41598-017-17427-6.PMID: 29230013
Molecules. 2017 Oct 27;22(11). pii: E1829.doi: 10.3390/molecules22111829.PMID: 29077044
J Cell Biochem. 2018 Feb;119(2):2231-2239.doi: 10.1002/jcb.26385. PMID: 28857247
Phytomedicine. 2018 Feb 1;40:37-47. doi:10.1016/j.phymed.2017.12.030PMID: 29496173
Calculate Dilution Ratios(Only for Reference)
* 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.
|Fitoterapia. 2015 Jun 2;105:26-36. |
|Human microsomal cyttrochrome P450-mediated reduction of oxysophocarpine, an active and highly toxic constituent derived from Sophora flavescens species, and its intestinal absorption and metabolism in rat.[Pubmed: 26045316]|
|Oxysophocarpine (OSC), an active and toxic quinolizidine alkaloid, is highly valued in Sophora flavescens Ait. and Subprostrate sophora Root. OSC is used to treat inflammation and hepatitis for thousands of years in China. |
METHODS AND RESULTS:
This study aims to investigate the CYP450-mediated reduction responsible for metabolizing OSC and to evaluate the absorption and metabolism of OSC in rat in situ. Four metabolites were identified, with sophocarpine (SC) as the major metabolite. SC formation was rapid in human and rat liver microsomes (HLMs and RLMs, respectively). The reduction rates in the liver are two fold higher than in the intestine, both in humans and rats. In HLMs, inhibitors of CYP2C9, 3A4/5, 2D6, and 2B6 had strong inhibitory effects on SC formation. Meanwhile, inhibitors of CYP3A and CYP2D6 had significant inhibition on SC formation in RLMs. Human recombinant CYP3A4/5, 2B6, 2D6, and 2C9 contributed significantly to SC production. The permeability in rat intestine and the excretion rates of metabolites were highest in the duodenum (p<0.05), and the absorbed amount of OSC in duodenum and jejunum was concentration-dependent. The metabolism could be significantly decreased by CYP3A inhibitor ketoconazole.
In conclusion, the liver was the main organ responsible for OSC metabolism. First-pass metabolism via CYP3A4/5, 2B6, 2D6, and 2C9 may be the main reason for the poor OSC bioavailability.
|Cell Mol Neurobiol. 2017 Mar;37(2):339-349. |
|The Anticonvulsant and Neuroprotective Effects of Oxysophocarpine on Pilocarpine-Induced Convulsions in Adult Male Mice.[Pubmed: 27481234]|
|Epilepsy is one of the prevalent and major neurological disorders, and approximately one-third of the individuals with epilepsy experience seizures that do not respond well to available medications. |
METHODS AND RESULTS:
We investigated whether Oxysophocarpine (OSC) had anticonvulsant and neuroprotective property in the pilocarpine (PILO)-treated mice. Thirty minutes prior to the PILO injection, the mice were administrated with OSC (20, 40, and 80 mg/kg) once. Seizures and electroencephalography (EEG) were observed, and then the mice were killed for Nissl and Fluoro-jade B (FJB) staining. The oxidative stress was measured at 24 h after convulsion. Western blot analysis was used to examine the expressions of the Bax, Bcl-2, and Caspase-3. In this study, we found that pretreatment with OSC (40, 80 mg/kg) significantly delayed the onset of the first convulsion and status epilepticus (SE) and reduced the incidence of SE and mortality. Analysis of EEG recordings revealed that OSC (40, 80 mg/kg) significantly reduced epileptiform discharges. Furthermore, Nissl and FJB staining showed that OSC (40, 80 mg/kg) attenuated the neuronal cell loss and degeneration in hippocampus. In addition, OSC (40, 80 mg/kg) attenuated the changes in the levels of Malondialdehyde (MDA) and strengthened glutathione peroxidase and catalase activity in the hippocampus. Western blot analysis showed that OSC (40, 80 mg/kg) significantly decreased the expressions of Bax, Caspase-3 and increased the expression of Bcl-2.
Collectively, the findings of this study indicated that OSC exerted anticonvulsant and neuroprotective effects on PILO-treated mice. The beneficial effects should encourage further studies to investigate OSC as an adjuvant in epilepsy, both to prevent seizures and to protect neurons in brain.