Schisandrin A

Catalog No.S3822 Batch:S382201

Technical Data

Formula	C₂₄H₃₂O₆
Molecular Weight	416.51	CAS No.	61281-38-7
Solubility (25°C)*	In vitro	DMSO	83 mg/mL (199.27 mM)


* <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations. * Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

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Biological Activity

Description

Schisandrin A (Sch A, Deoxyschizandrin, Wuweizisu A) is an active component of Schisandrae Fructus with liver-protective, antitumor, and antioxidant activities. It is an agonist of the adiponectin receptor 2 (AdipoR2) with the IC50 value of 3.5 μM.

Targets

AdipoR2 ^[4]

3.5 μM

In vitro

Schisandrin A significantly suppresses the lipopolysaccharide (LPS)-induced production of the key pro-inflammatory mediators nitric oxide (NO) and prostaglandin E2 by suppressing the expression of inducible NO synthase and cyclooxygenase-2 at the mRNA and protein levels in RAW 264.7 macrophages. It is demonstrated to reduce the LPS-induced secretion of pro-inflammatory cytokines, including tumor necrosis factor-α and interleukin-1β; this is accompanied by a simultaneous decrease in the respective mRNA and protein levels in the macrophages. In addition, the LPS- induced translocation of nuclear factor-κB (NF-κB), as well as activation of mitogen-activated protein kinases (MAPKs) and phosphatidylinositol-3 kinase (PI3K)/Akt pathways are inhibited by schisandrin A. These results suggest that schisandrin A has a protective effect against LPS-induced inflammatory and oxidative responses in RAW 264.7 cells by inhibiting the NF-κB, MAPK and PI3K/Akt pathways. Schisandrin A possesses anti-inflammatory activities and excellent Nrf2-induction or ROS-scavenging abilities^[2]. Schisandrin A can inhibit the replication of four serotypes of DENV in a concentration- and time-dependent manner, with an effective half-maximal effective concentration 50% (EC50) value of 28.1 ± 0.42 μM against DENV serotype type 2 without significant cytotoxicity^[3].

In vivo

Schisandrin A has proven beneficial in preventing cell damage in the pathogenesis of central nervous system diseases, including ischemia^[2]. Schisandrin A can effectively protect mice from DENV (Dengue virus) infection by reducing disease symptoms and mortality of DENV-infected mice. It stimulates IFN-mediated antiviral responses in vivo^[3].

Protocol (from reference)

Cell Assay:^{^[2]}	Cell lines The RAW 264.7 murine macrophage cell line Concentrations 0-200 μM Incubation Time 1 h Method To evaluate the cytotoxicity of schisandrin A, RAW 264.7 cells are seeded in 96-well plates at a density of 1×10³ cells/well. The cells are treated with various concentrations of schisandrin A for 1 h prior to incubation with LPS (100 ng/ml) for 24 h. After the incubation was complete, images of cells from each well are captured under a phase-contrast microscope. Subsequently, MTT is added to each well at 0.5 mg/ml, followed by incubation at 37°C in the dark. After 3 h of incubation, the MTT solution is removed and 200 μl 5% DMSO is added to dissolve the crystals. The viable cells are detected by reading the absorbance of formazan at 540 nm using an enzyme-linked immunosorbent assay (ELISA) microplate reader. The optical density of the formazan formed in the control (untreated) cells is considered to represent 100% viability.
Animal Study:^{^[1]}	Animal Models Male Kunming White mice Dosages 1, 10, 20 mg/kg d Administration intragastrically administrated

Cell Assay:^{^[2]}

Cell lines
The RAW 264.7 murine macrophage cell line
Concentrations
0-200 μM
Incubation Time
1 h
Method
To evaluate the cytotoxicity of schisandrin A, RAW 264.7 cells are seeded in 96-well plates at a density of 1×10³ cells/well. The cells are treated with various concentrations of schisandrin A for 1 h prior to incubation with LPS (100 ng/ml) for 24 h. After the incubation was complete, images of cells from each well are captured under a phase-contrast microscope. Subsequently, MTT is added to each well at 0.5 mg/ml, followed by incubation at 37°C in the dark. After 3 h of incubation, the MTT solution is removed and 200 μl 5% DMSO is added to dissolve the crystals. The viable cells are detected by reading the absorbance of formazan at 540 nm using an enzyme-linked immunosorbent assay (ELISA) microplate reader. The optical density of the formazan formed in the control (untreated) cells is considered to represent 100% viability.

Animal Study:^{^[1]}

Animal Models
Male Kunming White mice
Dosages
1, 10, 20 mg/kg d
Administration
intragastrically administrated

References

[4] Sun Y, et al. PLoS One. 2013, 8(5):e63354.

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SHIPPING AND STORAGE
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