||Schisandrin A , an agonist of the adiponectin receptor 2 (AdipoR2) with the IC50 value of 3.5 μM, has neuroprotective, anti-inflammatory, liver-protective, antitumor, and antioxidant activities. It alleviated microglia-mediated neuroinflammation injury through inhibiting the TRAF6-IKKβ-NF-κB and Jak2-Stat3 signaling pathways. It inhibited CYP3A activity with an IC50 of 6.60 μM and Ki of 5.83 μM, respectively.|
|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.
METHODS AND RESULTS:
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.
|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 AND RESULTS:
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.
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.