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J Chromatogr B Analyt Technol Bio...2020...Plant Cell Tiss Org2017, 479-486Plant Biotechnology Reports ...2021...Molecules.2020, 25(3):734J Food Compos Anal2017, 62:197-204Antioxidants (Basel)....2022...Front Pharmacol.2017, 8:673South African J of Botany...2020...
J Food Biochem.2020, 44(6):e13198. Primary and Industrial.2018, 52(11)Int J Mol Sci.2021, 22(16):8641.Eur J Neurosci.2021, 53(11):3548-3560.Phytomedicine.2019, 57:95-104Genes Genomics.2020, 10.1007Nutr Cancer.2023, 75(1):376-387.Korean Journal of Pharmacognosy....2015...
PLoS One.2022, 17(6):e0268505. Kasetsart University2022, ethesis.1144.Int J Mol Sci.2019, 20(3):E651Chem Biol Interact.2018, 290:44-51Eur J Pharmacol.2021, 899:174010. Toxicol Appl Pharmacol....2021...Pharmacogn Mag.2015, 11:S585-91
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J Korean Soc Food Sci Nutr2020, doi: 10.3746.J Food Sci.2022, 87(11):4905-4916.Curr Issues Mol Biol.2022, 44(5):2300-2308. FEBS Lett.2015, 589(1):182-7Pharmaceutics.2022, 14(3):564.J Chromatogr B Analyt Technol Biomed Life Sci.2019, 1124:323-330Molecules.2021, 26(9):2765. Biol Pharm Bull.2021, 44(12):1891-1893.Int J Mol Sci.2021, 22(16):8604.Front Pharmacol.2021, 12:762829.
Related Screening Libraries
||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. |
||ERK | JNK | P450 (e.g. CYP17) | p38MAPK | Caspase|
|Zhong Yao Cai. 2010 Mar;33(3):397-401. |
|Protective and therapeutic effects of schisandrol A on Abeta damaged PC12 cells.[Pubmed: 20681306]|
|To observe the protective and therapeutic effect of Schisandrol A on the Abeta damaged PC12 cells. PC12 cells were damaged by Abeta in vitro.
METHODS AND RESULTS:
Morphological changes were observed and the number of cells with neurite was analyzed by phase contrast microscope. The cell viability of PC12 cells was determined by the MTT method. Many dispirited cells with atrophied or fragmented neurites in the Abeta damaged PC12 cells were observed under the microscope. More vital cells with longer neurites were observed in the Schisandrol A treated PC12 cells and the number of cells with neurite increased. The difference of cell viability between the two groups was statistical significant.
Schisandrol A can antagonize the neurotoxicity of Abeta and has protective and therapeutic efficacy on Abeta damaged PC12 cells.
|Breast Cancer . 2018 Mar;25 |
|Schisandrin A reverses doxorubicin-resistant human breast cancer cell line by the inhibition of P65 and Stat3 phosphorylation[Pubmed: 29181822]|
|Background: Multidrug resistance (MDR) in breast cancer therapy occurs frequently. Thus, anti-MDR agents from natural products or synthetic compounds were tested extensively. We have also explored the reverse effect and mechanism of Schisandrin A (Sch A), a natural product, on MCF-7 breast cancer doxorubicin (DOX)-resistant subline MCF-7/DOX.
Methods: MTT assay was performed to measure the viability of MCF-7 cells to assess the reverse effect of Sch A. Western blot analysis was used to study the protein levels. Laser scanning confocal microscopy was performed to detect the intercellular DOX and Rhodamine 123 accumulation. The qRT-PCR was used to analysis the target gene expression. Dual-luciferase reporter assay was performed to test the transcriptional activity of P-glycoprotein (P-gp).
Results: Sch A, at the concentration of 20 μM, showed selective reverse effect (better than the positive control, verapamil at 5 μM) on MCF-7/DOX cell line but not on BEL-7402/DOX, Hep G2/DOX, and K-562/DOX cells. In addition, Sch A enhanced DOX-induced cleavage of Caspase-9 and PARP levels by increasing intracellular DOX accumulation and inhibiting P-gp function. Furthermore, Sch A selectively suppressed P-gp at gene and protein levels in MCF-7/DOX cells which express high level of MDR1 but not MRP1, MRP3, or BCRP. Besides, Sch A showed inhibitory effect on P-gp transcriptional activity. Sch A significantly reduced p-IκB-α (Ser32) and p-Stat3 (Tyr705) levels which mediate P-gp expression. In addition, Stat3 knockdown enhanced the reverse effect of siP65. The combined effect of siStat3 and siP65 was better than Sch A single treatment in MCF-7/DOX cells.
Conclusion: Sch A specifically reverses P-gp-mediated DOX resistance in MCF-7/DOX cells by blocking P-gp, NF-κB, and Stat3 signaling. Inhibition of P65 and Stat3 shows potent anti-MDR effect on MCF-7/DOX cells.
Keywords: Doxorubicin; Multidrug resistance; NF-κB; Schisandrin A; Stat3.|
|Cell Mol Biol (Noisy-le-grand). 2016 Mar 31;62(3):115-9. |
|Cavernosum smooth muscle relaxation induced by Schisandrol A via the NO-cGMP signaling pathway.[Pubmed: 27064883]|
|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).
METHODS AND RESULTS:
The pre-contracted penis with phenylephrine (Phe, 10 μM) was treated with accumulative concentrations of Schisandrol A (10-7, 10-6, 10-5 and 10-4 M). The change in intracavernosum pressure (ICP) and tension was recorded, cyclic nucleotides in the cavernosum tissue were measured by radioimmunoassay, mRNA level and expression of endothelial nitric oxide synthase (eNOS) and neuronal NOS (nNOS) were measured by real time PCR and western blot respectively.
The corpus cavernosum smooth muscle relaxation induced by Schisandrol A was in a dose-dependent manner. Pre-treatment with NOS inhibitor (Nω nitro-L-arginine-methyl ester, L-NAME) or guanylyl cyclase inhibitor (1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one, ODQ) significantly diminished the relaxation. The cyclic guanosine monophosphate (cGMP) level was significantly increased in the cavernosum tissue. Real time PCR and western blot showed the mRNA level and expression of eNOS and nNOS was also upregulated.
Schisandrol A relaxes the cavernosum smooth muscle by activating NO-cGMP signaling pathway. It may be a new promising treatment for erectile dysfunction and cardiovascular disease.
Schisandrol A Description
||The fruits of Schisandra chinensis (Turcz.) Baill.
||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.
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.IF=36.216(2019)PMID: 29328914
Cell Metab. 2020 Mar 3;31(3):534-548.e5. doi: 10.1016/j.cmet.2020.01.002.IF=22.415(2019)PMID: 32004475
Mol Cell. 2017 Nov 16;68(4):673-685.e6. doi: 10.1016/j.molcel.2017.10.022.IF=14.548(2019)PMID: 29149595
ACS Nano. 2018 Apr 24;12(4): 3385-3396. doi: 10.1021/acsnano.7b08969.IF=13.903(2019)PMID: 29553709
Nature Plants. 2016 Dec 22;3: 16206. doi: 10.1038/nplants.2016.205.IF=13.297(2019)PMID: 28005066
Sci Adv. 2018 Oct 24;4(10): eaat6994. doi: 10.1126/sciadv.aat6994.IF=12.804(2019)PMID: 30417089
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.
|Planta Med. 2007 Mar;73(3):212-20. |
|Schisandrol A from Schisandra chinensis reverses P-glycoprotein-mediated multidrug resistance by affecting Pgp-substrate complexes.[Pubmed: 17318783]|
|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.
METHODS AND RESULTS:
Through screening of herbs, we found that Schisandrol A (SCH) isolated from Fructus Schisandrae (the dried fruit of Schisandra chinensis (Turcz.) Baill.) sensitized Pgp-MDR HepG2-DR cells by interfering with the function of Pgp-substrate complexes. In Pgp-MDR cells, SCH enhanced the cytotoxicity of cancer drugs that are Pgp substrates and restored vinblastine-induced G2/M arrest without lowering Pgp expression. SCH increased cellular retention of Pgp substrates such as rhodamine 123. In Pgp-overexpressing membrane preparations, SCH stimulated basal Pgp-ATPase thus showing some substrate-like function. However, SCH was not a competitive inhibitor for verapamil or progesterone and decreased their Km. In the presence of substrates, SCH decreased the reactivity between Pgp and the monoclonal antibody UIC-2 which is normally increased with active substrate-Pgp complexes. The labeling of active Pgp transport sites by [125I]-iodoarylazidoprazosin was partially blocked by SCH.
SCH did not affect the activity of the mutant Pgp F983A suggesting that SCH acted differently than the thioxanthene type of Pgp allosteric inhibitors. Our results suggest that SCH acts by affecting the normal formation and functioning of the Pgp-substrate complexes.
|Phytomedicine. 2010 Jul;17(8-9):702-5. |
|Inhibition of cytochrome P450 3A4 activity by schisandrol A and gomisin A isolated from Fructus Schisandrae chinensis.[Pubmed: 20089387 ]|
|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.|
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