Schisandrin ACAS# 7432-28-2 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 7432-28-2 | SDF | Download SDF |
| PubChem ID | 23915 | Appearance | White powder |
| Formula | C24H32O7 | M.Wt | 432.5 |
| Type of Compound | Lignans | Storage | Desiccate at -20°C |
| Synonyms | Schizandrol; Schizandrol-A; Wuweizi alcohol-A; Wuweizichun-A | ||
| Solubility | DMSO : 1 mg/mL (2.31 mM; Need ultrasonic) | ||
| SMILES | CC1CC2=CC(=C(C(=C2C3=C(C(=C(C=C3CC1(C)O)OC)OC)OC)OC)OC)OC | ||
| Standard InChIKey | YEFOAORQXAOVJQ-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C24H32O7/c1-13-9-14-10-16(26-3)20(28-5)22(30-7)18(14)19-15(12-24(13,2)25)11-17(27-4)21(29-6)23(19)31-8/h10-11,13,25H,9,12H2,1-8H3 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Schisandrol A may be a new promising treatment for neurotoxicity, erectile dysfunction and cardiovascular disease.It can inhibit the activities of Pgp,Beta Amyloid,CYP3A4,cGMP,and NOS, the IC(50) value of CYP3A4 is 32.02 microM. |
| Targets | ERK | JNK | P450 (e.g. CYP17) | p38MAPK | Caspase |
| In vitro | Protective and therapeutic effects of schisandrol A on Abeta damaged PC12 cells.[Pubmed: 20681306]Zhong Yao Cai. 2010 Mar;33(3):397-401.To observe the protective and therapeutic effect of Schisandrol A on the Abeta damaged PC12 cells. PC12 cells were damaged by Abeta in vitro.
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| In vivo | Cavernosum smooth muscle relaxation induced by Schisandrol A via the NO-cGMP signaling pathway.[Pubmed: 27064883]Cell Mol Biol (Noisy-le-grand). 2016 Mar 31;62(3):115-9.To evaluate the effect of Schisandrol A on rabbit corpus cavernosum smooth muscle and elucidate the potential mechanism. Penises were obtained from healthy male New Zealand White rabbits (2.5-3.0 kg).
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| Cell Research | Inhibition of cytochrome P450 3A4 activity by schisandrol A and gomisin A isolated from Fructus Schisandrae chinensis.[Pubmed: 20089387 ]Schisandrol A from Schisandra chinensis reverses P-glycoprotein-mediated multidrug resistance by affecting Pgp-substrate complexes.[Pubmed: 17318783]Planta Med. 2007 Mar;73(3):212-20.Recent studies have shown that dibenzocyclooctadiene lignans may reverse P-glycoprotein-mediated multidrug resistance (Pgp-MDR) in cancer cells; however, the mechanism of action remains unknown.
Phytomedicine. 2010 Jul;17(8-9):702-5.We studied the effects of Schisandrol A (SCH) and gomisin A (GOM), two of the main bioactive components of Fructus Schisandrae chinensis, on cytochrome P450-3A4 (CYP3A4) activity and cellular glutathione (GSH) level. In a cell-free system both SCH and GOM inhibited CYP3A4 activity with IC(50) values of 32.02 microM and 1.39 microM, respectively. SCH or GOM at concentrations up to 100 microM did not alter cellular GSH level in regular HepG2 cells and P-glycoprotein overexpressing HepG2-DR cells. Since SCH and GOM may reverse multidrug resistance (MDR) by impeding the activity of P-glycoprotein, a membrane xenobiotic exporter, SCH or GOM could affect cellular drug metabolism in addition to drug uptake. |
Schisandrin A Dilution Calculator
Schisandrin A Molarity Calculator
| 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 |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Schisandrin has various therapeutic effects on a range of medical conditions such as anti-asthmatic, anti-cancer, and anti-inflammatory effects. IC50 value: Target: in vitro: Sch inhibited the pro-fibrotic activity of TGF-β1 in AML12 cells; thus, it suppressed the accumulation of ECM proteins. Also, Sch inhibited the EMT as assessed by reduced expression of vimentin and fibronectin, and increased E-cadherin and ZO-1 in TGF-β1 induced AML12 cells. Sch reduced TGF-β1-mediated phosphorylation of Smad2/3 and Smad3/4 DNA binding activity. On the other hand, Sch reduced TGF-β1-induced ERK1/2 and PI3K/Akt phosphorylation in the non-Smad pathway [1]. the anti-inflammatory properties of schisandrin result from the inhibition of nitric oxide (NO) production, prostaglandin E(2) (PGE(2)) release, cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) expression, which in turn results from the inhibition of nuclear factor-kappaB (NF-kappaB), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) activities in a RAW 264.7 macrophage cell line [2].
References:
[1]. Park JH, et al. Schizandrin inhibits fibrosis and epithelial-mesenchymal transition in transforming growth factor-β1-stimulated AML12 cells. Int Immunopharmacol. 2015 Apr;25(2):276-84.
[2]. Guo LY, et al. Anti-inflammatory effects of schisandrin isolated from the fruit of Schisandra chinensis Baill. Eur J Pharmacol. 2008 Sep 4;591(1-3):293-9.
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Schisandrin A and B affect subventricular zone neurogenesis in mouse.[Pubmed:24975096]
Eur J Pharmacol. 2014 Oct 5;740:552-9.
Schisandrin A and B (Sch A and B) are the main effective components extracted from the oriental medicine Schisandra chinensis which is traditionally used to enhance mental and intellectual function. Although their neuroprotective effects have been demonstrated, their influences on neurogenesis are still unknown. In the brain, new neural cells born in the subventricular zone (SVZ) next to the lateral ventricles migrate along the rostral migratory stream (RMS) to the olfactory bulb (OB). To investigate the effects of Sch A and B on neurogenesis in the SVZ-RMS-OB system, Sch A and B were intragastrically administrated at dosages of 1, 10 and 20 mg/kg d respectively. The dose of 10 mg/kg d was selected for further analysis based on the preliminary analysis. In the SVZ, significant increases of phosphohistone H3 positive proliferating cells and the intensity of glial fibrillary acidic protein (GFAP+) cells were noticed in Sch B group. In the RMS, Sch A treatment augmented the intensity of doublecortin positive neuroblasts. In the OB, Sch A decreased tyrosine hydroxylase cells and Calbindin (CalB+) cells, while Sch B increased CalB+ cells and Calretinin (CalR+) cells. These results suggest that Sch B stimulates SVZ proliferation by enhancing GFAP+ cells and improves the survival of OB interneurons, while Sch 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 Sch A mainly negatively regulates neurogenesis, in the adult SVZ-RMS-OB system.
Neuroprotective effect of schizandrin A on oxygen and glucose deprivation/reperfusion-induced cell injury in primary culture of rat cortical neurons.[Pubmed:24986222]
J Physiol Biochem. 2014 Sep;70(3):735-47.
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.
The protective mechanism of schisandrin A in d-galactosamine-induced acute liver injury through activation of autophagy.[Pubmed:24992201]
Pharm Biol. 2014 Oct;52(10):1302-7.
CONTEXT: The principal bioactive lignan of Schisandra chinensis fructus, commonly used for traditional Chinese medicine, is Schisandrin A. Schisandrin A has been widely reported as being very effective for the treatment of liver disease. However, the mechanisms of its protective effects in liver remain unclear. OBJECTIVE: To explore the hepatoprotective mechanisms of Schisandrin A. MATERIALS AND METHODS: d-Galactosamine (d-GalN)-induced liver injury in mice was used as a model. Schisandrin A was examined for its protective mechanisms using hematoxylin-eosin (HE) staining, enzyme-linked immunosorbent assay (ELISA), western blotting and real-time PCR (RT-PCR). RESULTS: 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. CONCLUSION: Our results show that the hepatoprotective mechanisms of Schisandrin A may include activation of autophagy flux and inhibition of apoptosis. These results provide pharmacological evidence supporting its future clinical application.
Identification of CYP2C19 inhibitors from phytochemicals using the recombinant human enzyme model.[Pubmed:24855828]
Pharmazie. 2014 May;69(5):362-6.
The aim of the present study was to develop the recombinant insect cell-expressed protein as an in vitro model for inhibitors screening for human cytochrome P450 2C19 (CYP2C19), and to use the model to investigate the inhibition effect of three phytochemicals on CYP2C19 in vitro. Omeprazole was applied as the probe substrate. The estimated inhibitory constant (K(i)) of ticlopidine and fluvoxamine were 0.64 +/- 0.025 microM and 0.29 +/- 0.090 microM, respectively. After co-incubation with ticlopidine or fluvoxamine, the mean omeprazole Michaelis-Menten constant (K(m)) increased from 4.99 +/- 0.22 microM to 16.25 +/- 1.22 microM or 19.20 +/- 1.73 microM, respectively, while omeprazole's mean V(max) did not vary much. Both ticlopidine and fluvoxamine were competitive inhibitors of CYP2C19. 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.
