|Source:||The fruits of Schisandra chinensis (Turcz.) Baill.|
|Biological Activity or Inhibitors:||1. Schisandrol A has hepatoprotective activity.
2. Schisandrol A is a potent P-gp inhibitor.
3. Schisandrol A, as an inhibitor of CYP3A, possesses a clinically beneficial property of altering the disposition of drugs metabolized by CYP3A.
4. Schisandrol A demonstrates strong and comparable activities to reverse the drug resistance and the intracellular drug accumulation in four mediated multidrug resistance (MDR) cell lines.
|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: email@example.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.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||2.3121 mL||11.5607 mL||23.1214 mL||46.2428 mL||57.8035 mL|
|5 mM||0.4624 mL||2.3121 mL||4.6243 mL||9.2486 mL||11.5607 mL|
|10 mM||0.2312 mL||1.1561 mL||2.3121 mL||4.6243 mL||5.7803 mL|
|50 mM||0.0462 mL||0.2312 mL||0.4624 mL||0.9249 mL||1.1561 mL|
|100 mM||0.0231 mL||0.1156 mL||0.2312 mL||0.4624 mL||0.578 mL|
J Physiol Biochem. 2014 Sep;70(3):735-47.
|Neuroprotective effect of schizandrin A on oxygen and glucose deprivation/reperfusion-induced cell injury in primary culture of rat cortical neurons.[Pubmed: 24986222]|
|The results showed that schizandrin A significantly reduced cell apoptosis and necrosis, increased cell survival, and decreased intracellular calcium concentration ([Ca(2+)]i) and lactate dehydrogenase (LDH) release in primary culture of rat cortical neurons after OGD/R. Mechanism studies suggested that the modulation of extracellular-regulated kinase (ERK), c-Jun NH2-terminal kinases (JNK), and p38, as well as caspase-3 activity played an important role on the progress of neuronal apoptosis. C5aR participated in the neuroprotective effect of schizandrin A in primary culture of rat cortical neurons after OGD/R. Our findings suggested that schizandrin A might act as a candidate therapeutic target drug used for brain ischemia and related diseases.|
Pharm Biol. 2014 Oct;52(10):1302-7.
|The protective mechanism of schisandrin A in d-galactosamine-induced acute liver injury through activation of autophagy.[Pubmed: 24992201]|
|Aspartate amino-transferase (AST) and alanine transaminase (ALT) levels in the schisandrin A group were significantly decreased (p < 0.01) compared with those in the d-GalN-treated group. HE results showed that the pathological changes in hepatic tissue seen in the d-GalN-treated were reduced in the schisandrin A/d-GalN-treated group, with the morphological characteristics being close to those of the control (untreated) group. Western blotting results showed that schisandrin A can activate autophagy flux and inhibit progression of apoptosis. The immune function of the schisandrin A-pretreated group was assayed by flow cytometry. It was found that the mechanism may involve activated autophagy flux, inhibited apoptosis, and improved immunity in response to liver damage.|
Eur J Pharmacol. 2014 Oct 5;740:552-9.
|Schisandrin A and B affect subventricular zone neurogenesis in mouse.[Pubmed: 24975096]|
|These results suggest that Schisandrin B stimulates SVZ proliferation by enhancing GFAP+ cells and improves the survival of OB interneurons, while Schisandrin A promotes neuroblast formation in the RMS but impairs the survival of OB interneurons. The present study provides the first evidence that Sch B exerts neuroprotective functions by enhancing neurogenesis, but Schisandrin A mainly negatively regulates neurogenesis, in the adult SVZ-RMS-OB system.|
Pharmazie. 2014 May;69(5):362-6.
|Identification of CYP2C19 inhibitors from phytochemicals using the recombinant human enzyme model.[Pubmed: 24855828]|
|The IC50 of three phytochemicals, isoalantolactone, curcumol and schisandrin A was determined as 38.91 microM, 121.0 microM and 86.41 microM, and the K(i) as 5.02 +/- 1.04 microM, 35.84 +/- 8.95 microM, and 4.46 +/- 0.017 microM, respectively. The in vitro model for inhibitor screening established using recombinant CYP2C19 could be used to assess the inhibition potential of drug candidates. Isoalantolactone and schisandrin A are potent inhibitors of CYP2C19, while curcumol is a moderate potent inhibitor of CYP2C19.|