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Int J Oncol. 2016 Oct;49(4)Acta Biochim Pol.2015 May 26Mol Med Rep.2014 May;9(5):1653-9.Mol Cells.2015 Sep 30;38(9):765-72.J. Acta Agr. Scandinavica17 Apr 2017
Yakugaku Zasshi.2018 Jan 30;Acta Pharmaceutica Sinica B2015 Apr.7.Int J Mol Sci. 2018 Jan 23;Phytomedicine15 Dec. 2015,1262–1268Phytochemistry Letters22 Dec. 2016
Int. J. of Food Properties08 Feb 2017;Auburn, Alabama2015 Aug 1J Agric Food Chem.2018 Jan 10;Cell Physiol Biochem. 2017;44(4);
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||p-Synephrine is widely used in weight loss and weight management as well as in sports performance products, which has antidepressant-like effects in the murine models of forced swimming and tail suspension, it also exerts potent anti-inflammatory effects by inhibition of the NF-κB signaling pathway. Synephrine inhibits eotaxin-1 expression via the STAT6 signaling pathway.|
||STAT | IL Receptor | JAK | NF-kB | p65 | IkB | cAMP | Calcium Channel | IKK|
|Molecules. 2014 Aug 8;19(8):11883-95. |
|Synephrine inhibits eotaxin-1 expression via the STAT6 signaling pathway.[Pubmed: 25111027]|
|Citrus contain various flavonoids and alkaloids that have multiple biological activities. It is known that the immature Citrus contains larger amounts of bioactive components, than do the mature plants. Although Citrus flavonoids are well known for their biological activities, Citrus alkaloids have not previously been assessed.
METHODS AND RESULTS:
In this study, we identified Synephrine alkaloids as an active compound from immature Citrus unshiu, and investigated the effect of Synephrine on eotaxin-1 expression. Eotaxin-1 is a potent chemoattractant for eosinophils, and a critical mediator, during the development of eosinophilic inflammation. We found that Synephrine significantly inhibited IL-4-induced eotaxin-1 expression. This Synephrine effect was mediated through the inhibition of STAT6 phosphorylation in JAK/STAT signaling. We also found that eosinophil recruitment induced by eotaxin-1 overexpression was inhibited by Synephrine.
Taken together, these findings indicate that inhibiting IL-4-induced eotaxin-1 expression by Synephrine occurs primarily through the suppression of eosinophil recruitment, which is mediated by inhibiting STAT6 phosphorylation.
|Mol Cell Biochem. 2014 Mar;388(1-2):135-47. |
|The action of p-synephrine on hepatic carbohydrate metabolism and respiration occurs via both Ca(2+)-mobilization and cAMP production.[Pubmed: 24287564]|
|Citrus aurantium extracts, which contain large amounts of p-Synephrine, are widely used for weight loss purposes and as appetite suppressants. In the liver, C. aurantium (bitter orange) extracts affect hemodynamics, carbohydrate metabolism, and oxygen uptake. The purpose of the present work was to quantify the action of p-Synephrine and also to obtain indications about its mechanism of action, a task that would be difficult to accomplish with C. aurantium extracts due to their rather complex composition.
METHODS AND RESULTS:
The experimental system was the isolated perfused rat liver. p-Synephrine significantly stimulated glycogenolysis, glycolysis, gluconeogenesis, and oxygen uptake. The compound also increased the portal perfusion pressure and the redox state of the cytosolic NAD(+)/NADH couple. A Ca(2+)-dependency for both the hemodynamic and the metabolic effects of p-Synephrine was found. p-Synephrine stimulated both cAMP overflow and the initial Ca(2+) release from the cellular stores previously labeled with (45)Ca(2+). The metabolic and hemodynamic actions of p-Synephrine were strongly inhibited by α-adrenergic antagonists and moderately affected by β-adrenergic antagonists.
The results allow to conclude that p-Synephrine presents important metabolic and hemodynamic effects in the liver. These effects can be considered as both catabolic (glycogenolysis) and anabolic (gluconeogenesis), they are mediated by both α- and β-adrenergic signaling, require the simultaneous participation of both Ca(2+) and cAMP, and could be contributing to the overall stimulation of metabolism that usually occurs during weight loss periods.
|Inflamm Res. 2014 Jun;63(6):429-39. |
|p-Synephrine suppresses lipopolysaccharide-induced acute lung injury by inhibition of the NF-κB signaling pathway.[Pubmed: 24487736]|
|We investigated whether p-Synephrine exerts potent anti-inflammatory effects against acute lung injury (ALI) induced by lipopolysaccharide (LPS) in vivo, and we further investigated the inhibitory mechanism of p-Synephrine in LPS-induced ALI.
METHODS AND RESULTS:
Lipopolysaccharide (0.5 mg/kg) was instilled intranasally in phosphate-buffered saline to induce acute lung injury, and 6, 24, and 48 h after LPS was given, bronchoalveolar lavage fluid was obtained to measure pro-inflammatory mediator. We also evaluated the effects of p-Synephrine on LPS-induced the severity of pulmonary injury. The phosphorylation of nuclear factor-κB (NF-κB) p65 protein was analyzed by Western blotting.
Our data showed that p-Synephrine significantly reduced the amount of inflammatory cells, the lung wet-to-dry weight (W/D) ratio, reactive oxygen species, myeloperoxidase activity and enhanced superoxide dismutase (SOD) in mice with LPS-induced ALI. Tumor necrosis factor α and interleukin (IL)-6 concentrations decreased significantly while the concentration of IL-10 was significantly increased after p-Synephrine pretreatment. In addition, p-Synephrine suppressed not only the phosphorylation of NF-κB but also the degradation of its inhibitor (IκBα).
These results suggested that the inhibition of NF-κB activation and the regulation of SOD are involved in the mechanism of p-Synephrine's protection against ALI.
||The young fruits Citrus aurantium L.
||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.2017.12.030.PMID: 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.
|Naunyn Schmiedebergs Arch Pharmacol. 2001 Jul;364(1):21-6. |
|Characterization of antidepressant-like effects of p-synephrine stereoisomers.[Pubmed: 11485034]|
|We previously reported that p-Synephrine has antidepressant-like activity in the murine models of forced swimming and tail suspension.
METHODS AND RESULTS:
In the present study, we characterized antidepressant-like effects of p-Synephrine stereoisomers in both in vivo and in vitro systems. In the tail suspension test, S-(+)-p-Synephrine (3 mg/kg, p.o.) reduced the duration of immobility, while R-(-)-p-Synephrine (0.3-3 mg/kg, p.o.) had no effect. S-(+)-p-Synephrine (0.3, 1 and 3 mg/kg, p.o.) and R-(-)-p-Synephrine (1 mg/ kg and 3 mg/kg, p.o.) significantly reversed the reserpine (2.5 mg/kg, i.p.)-induced hypothermia. S-(+)-p-Synephrine was more effective than R-(-)-p-Synephrine in inhibition of both [3H]noradrenaline uptake in rat cerebral cortical slices (maximal inhibition 85.7 +/- 7.8% vs. 59.8 +/- 4.3%; EC50 5.8 +/- 0.7 microM vs. 13.5 +/- 1.2 microM) and [3H]nisoxetine binding (Ki 4.5 +/- 0.5 microM vs. 8.2 +/- 0.7 microM). In contrast, R-(-)-p-Synephrine was more effective than S-(+)-p-Synephrine in stimulation of [3H]noradrenaline release from rat cerebral cortical slices (maximal stimulation 23.9 +/- 1.8% vs. 20.1 +/- 1.7%; EC50 8.2 +/- 0.6 microM vs. EC50 12.3 +/- 0.9 microM). The stimulatory effect of R-(-)-p-Synephrine on [3H]noradrenaline release was inhibited by nisoxetine (100 nM), but tetrodotoxin (1 microM) and elimination of extracellular calcium had no effect.
It is suggested that S-(+)-p-Synephrine has more effective antidepressant-like activity than R-(-)-p-Synephrine.