|Source:||The seeds of Schisandra chinensis (Turcz.) Baill.|
|Biological Activity or Inhibitors:||1. Schizandrin A has neuroprotective effect on oxygen and glucose deprivation/
Reperfusion-induced cell injury in primary culture of rat cortical neurons, it may act as a candidate therapeutic target drug used for brain ischemia and related diseases.
2. Schizandrin A has the reversal effect of drug resistance in different mechanisms of the two cell lines of K562/ADR and HL60/ADR, it increases the concentration of the drug resistant cells mainly by inhibiting the function and expression of P-gp,MRP1 protein and reducing mdr1,mrp1 gene expression and GSH content.
3. Schizandrin A can exert anti-inflammatory and neuroprotective effects by alleviating microglia-mediated neuroinflammation injury through inhibiting the TRAF6-IKKβ-NF-κB and Jak2-Stat3 signaling pathways.
4. Schizandrin A is able to inhibit CYP3A activity in rat liver microsomes, the inhibition is mixed type,non-competitive and anti-competitive inhibition.
|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||2.4009 mL||12.0045 mL||24.009 mL||48.0181 mL||60.0226 mL|
|5 mM||0.4802 mL||2.4009 mL||4.8018 mL||9.6036 mL||12.0045 mL|
|10 mM||0.2401 mL||1.2005 mL||2.4009 mL||4.8018 mL||6.0023 mL|
|50 mM||0.048 mL||0.2401 mL||0.4802 mL||0.9604 mL||1.2005 mL|
|100 mM||0.024 mL||0.12 mL||0.2401 mL||0.4802 mL||0.6002 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]|
|Brain ischemia appears to be associated with innate immunity. Recent reports showed that C3a and C5a, as potent targets, might protect against ischemia induced cell death. In traditional Chinese medicine, the fruit of Schizandra chinesis Baill (Fructus schizandrae) has been widely used as a tonic. In the present study, we sought to evaluate the neuroprotective effects of Schizandrin A, a composition of S. chinesis Baill, against oxygen and glucose deprivation followed by reperfusion (OGD/R)-induced cell death in primary culture of rat cortical neurons, and to test whether C3a and C5a affected cortical neuron recovery from ischemic injury after Schizandrin A treatment. 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.|
PLoS One. 2016 Feb 26;11(2):e0149991.
|Schizandrin A Inhibits Microglia-Mediated Neuroninflammation through Inhibiting TRAF6-NF-κB and Jak2-Stat3 Signaling Pathways.[Pubmed: 26919063]|
|Microglial-mediated neuroinflammation has been established as playing a vital role in pathogenesis of neurodegenerative disorders. Thus, rational regulation of microglia functions to inhibit inflammation injury may be a logical and promising approach to neurodegenerative disease therapy. The purposes of the present study were to explore the neuroprotective effects and potential molecular mechanism of Schizandrin A (Sch A), a lignin compound isolated from Schisandra chinesnesis. Our observations showed that Sch A could significantly down-regulate the increased production of nitric oxide (NO), tumor necrosis factor (TNF)-α and interleukin (IL)-6 induced by lipopolysaccharide (LPS) both in BV-2 cells and primary microglia cells. Moreover, Sch A exerted obvious neuroprotective effects against inflammatory injury in neurons when exposed to microglia-conditioned medium. Investigations of the mechanism showed the anti-inflammatory effect of Sch A involved the inhibition of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2) expression levels and inhibition of the LPS-induced TRAF6-IKKβ-NF-κB pathway. Furthermore, inhibition of Jak2-Stat3 pathway activation and Stat3 nuclear translocation also was observed. In conclusion, SchA can exert anti-inflammatory and neuroprotective effects by alleviating microglia-mediated neuroinflammation injury through inhibiting the TRAF6-IKKβ-NF-κB and Jak2-Stat3 signaling pathways.|
Chinese Pharmacological Bulletin, 2011, 27(3): 329-34.
|Reversing mechanism of schizandrin A on multi-drug resistance of K562/ADR,HL60/ADR,MCF-7/ADR cell lines.[Reference: WebLink]|
|To study the reversal effect of Schizandrin A(schA) on the K562/ADR,HL60/ADR,MCF-7/ADR,and explore its reversal mechanism.Methods schA′s reversal effect was evaluated by MTT assay;accumulation of daunorubicin(DNR)and rhodamine-123(Rh123)and the expression of P-glycoprotein and multidrug resistance associated protein 1(MRP1)were evaluated by flow cytometry(FCM);the expression of intracellular mdr1 mRNA and mrp1 mRNA was detected with Real-time PCR;the changes of GSH content were detected by biochemical tests.Results The result of reversion of multidrug resistance showed schA had different reversal effects on different mechanisms of chemotherapeutic agents;the experiments of accumulation showed that the schA could significantly increase daunorubicin,rhodamine 123 contents in resistant cells,which had a good dose dependent effect;the treatment of schA could reduce remarkably the expressions of the P-gp protein and mdr1,mrp1 gene after 24 h treatment;and it could reduce GSH content after 4 h treatment in K562/ADR,HL60/ADR.Conclusions schA has the reversal effect of drug resistance in different mechanisms of the two cell lines of K562/ADR and HL60/ADR.It increases the concentration of the drug resistant cells mainly by inhibiting the function and expression of P-gp,MRP1 protein and reducing mdr1,mrp1 gene expression and GSH content,and then it enhances the sensitivity and reversal effects of resistant cell lines.|
Chinese Journal of Clinical Pharmacology & Therapeutics, 2009, 14(11):1275-80.
|Effects of schizandrin A on the activity of CYP3A in rat liver microsomes.[Reference: WebLink]|
|To study the effects of Schizandrin A on CYP3A by in vitro drug metabolism experiments.METHODS:Midazolam(MDZ)was adopted as a drug "probe" and a detection method of high-performance liquid chromatography(HPLC)was established,the rat liver microsome was as a carrier.The IC50 value of Schizandrin A by in vitro administration and related enzyme kinetic parameters on CYP3A were detected.RESULTS:The endogenous substances did not interfere with the determination in the incubation system.The method was fast,stable and had high sensitivity.The IC50 of Schizandrin A on MDZ metabolism in liver microsomes was 6.26 μmol/mL,and the enzyme kinetic parameters were as follows:Km=15.77 μmol/L,Ki=5.5 μmol/mL.CONCLUSION:Schizandrin A is able to inhibit CYP3A activity in rat liver microsomes.The inhibition is mixed type,non-competitive and anti-competitive inhibition.|