Schizandrin
(Synonyms: 五味子醇甲; Schizandrin; Schizandrol; Schizandrol-A) 目录号 : GC49674
A lignan with diverse biological activities
Cas No.:7432-28-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >97.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Schizandrin is a dibenzocyclooctadiene lignan and a major component of S. chinensis and has diverse biological activities.1,2,3,4,5 It induces cell cycle arrest at the G0/G1 phase and inhibits growth of T47D and MDA-MB-231 breast cancer cells when used at a concentration of 100 μM.1 Schizandrin (10 and 100 μM) prevents glutamate-induced cytotoxicity, inhibits production of nitric oxide (NO) and reactive oxygen species (ROS), and preserves the mitochondrial membrane potential in isolated rat cortical cells.2 It reduces apoptosis induced by cisplatin in HK-2 human kidney cells.3 In vivo, schizandrin (1 and 10 mg/kg, p.o.) reverses scopolamine-induced impairment of spatial memory and the passive avoidance response in rats.4 It enhances oxotremorine-induced tremors in mice. Schizandrin (10 mg/kg) reduces serum levels of IgE, IgG1, IL-4, and IFN-γ in an ovalbumin-sensitized mouse model of allergy.5
1.Kim, S.-J., Min, H.-Y., Lee, E.J., et al.Growth inhibition and cell cycle arrest in the G0/G1 by schizandrin, a dibenzocyclooctadiene lignan isolated from Schisandra chinensis, on T47D human breast cancer cellsPhytother. Res.24(2)193-197(2010) 2.Cheng, H.-Y., Hsieh, M.-T., Wu, C.-R., et al.Schizandrin protects primary cultures of rat cortical cells from glutamate-induced excitotoxicityJ. Pharmacol. Sci.107(1)21-31(2008) 3.Bunel, V., Antoine, M.-H., Nortier, J., et al.Protective effects of schizandrin and schizandrin B towards cisplatin nephrotoxicity in vitroJ. Appl. Toxicol.34(12)1311-1319(2013) 4.Egashira, N., Kurauchi, K., Iwasaki, K., et al.Schizandrin reverses memory impairment in ratsPhytother. Res.22(1)49-52(2008) 5.Han, N.-R., Moon, P.-D., Kim, N.-R., et al.Schisandra chinensis and its main constituent schizandrin attenuate allergic reactions by down-regulating caspase-1 in ovalbumin-sensitized miceAm. J. Chin. Med.45(1)159-172(2017)
| Cas No. | 7432-28-2 | SDF | Download SDF |
| 别名 | 五味子醇甲; Schizandrin; Schizandrol; Schizandrol-A | ||
| Canonical SMILES | COC1=C(OC)C(OC)=CC2=C1C3=C(C=C(OC)C(OC)=C3OC)C[C@@](O)(C)[C@@H](C)C2 | ||
| 分子式 | C24H32O7 | 分子量 | 432.5 |
| 溶解度 | DMF: 30 mg/ml,DMF:PBS(pH7.2) (1:2): 0.3 mg/ml,DMSO: 5 mg/ml,Ethanol: 2 mg/ml | 储存条件 | -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.3121 mL | 11.5607 mL | 23.1214 mL |
| 5 mM | 0.4624 mL | 2.3121 mL | 4.6243 mL |
| 10 mM | 0.2312 mL | 1.1561 mL | 2.3121 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Schizandrin A can inhibit non‑small cell lung cancer cell proliferation by inducing cell cycle arrest, apoptosis and autophagy
Int J Mol Med 2021 Dec;48(6):214.PMID:34643254DOI:10.3892/ijmm.2021.5047.
Schizandrin A (SchA) can be extracted from the vine plant Schisandra chinensis and has been reported to confer various biologically active properties. However, its potential biological effects on non‑small cell lung cancer (NSCLC) remain unknown. Therefore, the present study aims to address this issue. NSCLC and normal lung epithelial cell lines were first treated with SchA. Cell viability and proliferation were measured using CellTiter‑Glo Assay and colony formation assays, respectively. PI staining was used to measure cell cycle distribution. Cell cycle‑related proteins p53, p21, cyclin D1, CDK4, CDK6, cyclin E1, cyclin E2, CDK2 and DNA damage‑related protein SOX4 were detected by western blot analysis. Annexin V‑FITC/PI staining, DNA electrophoresis and Hoechst 33342/PI dual staining were used to detect apoptosis. JC‑1 and DCFH‑DA fluorescent dyes were used to measure the mitochondrial membrane potential and reactive oxygen species concentrations, respectively. Apoptosis‑related proteins caspase‑3, cleaved caspase‑3, poly(ADP‑ribose) polymerase (PARP), cleaved PARP, BimEL, BimL, BimS, Bcl2, Bax, caspase‑9 and cleaved caspas‑9 were measured by western blot analysis. Dansylcadaverine was used to detect the presence of the acidic lysosomal vesicles. The expression levels of the autophagy‑related proteins LC3‑I/II, p62/SQSTM and AMPKα activation were measured using western blot analysis. In addition, the autophagy inhibitor 3‑methyladenine was used to inhibit autophagy. SchA treatment was found to reduce NSCLC cell viability whilst inhibiting cell proliferation. Low concentrations of SchA (10‑20 µM) mainly induced G1/S‑phase cell cycle arrest. By contrast, as the concentration of SchA used increases (20‑50 µM), cells underwent apoptosis and G2/M‑phase cell cycle a13rrest. As the treatment concentration of SchA increased from 0 to 50 µM, the expression of p53 and SOX4 protein also concomitantly increased, but the expression of p21 protein was increased by 10 µM SchA and decreased by higher concentrations (20‑50 µM). In addition, the mRNA and protein expression levels of Bcl‑like 11 (Bim)EL, BimL and BimS increased following SchA application. SchA induced the accumulation of acidic vesicles and induced a marked increase in the expression of LC3‑II protein, suggsting that SchA activated the autophagy pathway. However, the expression of the p62 protein was found to be increased by SchA, suggesting that p62 was not degraded during the autophagic flux. The 3‑methyladenine exerted no notable effects on SchA‑induced apoptosis. Taken together, results from the present study suggest that SchA exerted inhibitory effects on NSCLC physiology by inducing cell cycle arrest and apoptosis. In addition, SchA partially induced autophagy, which did not result in any cytoprotective effects.
Schizandrin Protects against OGD/R-Induced Neuronal Injury by Suppressing Autophagy: Involvement of the AMPK/mTOR Pathway
Molecules 2019 Oct 8;24(19):3624.PMID:31597329DOI:10.3390/molecules24193624.
The neuroprotective role of Schizandrin (SA) in cerebral ischemia-reperfusion (I/R) was recently highlighted. However, whether SA plays a regulatory role on autophagy in cerebral I/R injury is still unclear. This study aimed to explore whether the neuroprotective mechanisms of SA were linked to its regulation of AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR)/autophagy pathway in vivo and in vitro. The present study confirmed that SA significantly improved oxygen-glucose deprivation/re-oxygenation (OGD/R)-induced PC12 cells injury. The results of immunoblotting and confocal microscope showed that SA decreased autophagy in OGD/R-injured PC12 cells, which was reflected by the decreased Beclin-1 and LC3-II expression, autophagy flux level, and LC3 puncta formation. In addition, the autophagy inducer rapamycin partially prevented the effects of SA on cell viability and autophagy after OGD/R, whereas the autophagy inhibitor 3-methyladenine (3-MA) exerted the opposite effect. The results of Western blotting showed that SA markedly decreased the phosphorylation of AMPK (p-AMPK), whereas the phosphor-mTOR (p-mTOR) levels increased in the presence of OGD/R insult. Furthermore, pretreatment with the AMPK inducer AICAR partially reversed the protective effects and autophagy inhibition of SA. However, AMPK inhibitor Compound C pretreatment further promoted the inhibition of SA on autophagy induction and cell damage induced by OGD/R. Taken together, these findings demonstrate that SA protects against OGD/R insult by inhibiting autophagy through the regulation of the AMPK-mTOR pathway and that SA may have therapeutic value for protecting neurons from cerebral ischemia.
Schizandrin B attenuates hypoxia/reoxygenation injury in H9c2 cells by activating the AMPK/Nrf2 signaling pathway
Exp Ther Med 2021 Mar;21(3):220.PMID:33603829DOI:10.3892/etm.2021.9651.
Schizandrin B exhibits prominent antioxidant and anti-inflammatory effects, and plays an important role in ameliorating myocardial ischemia/reperfusion injury. However, the underlying protective mechanisms remain to be elucidated. The aim of the present study was to explore the cardioprotective effects of Schizandrin B against hypoxia/reoxygenation (H/R)-induced H9c2 cell injury, focusing on the role of the adenosine monophosphate-activated protein kinase (AMPK)/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in this process. The results showed that Schizandrin B attenuated the H/R-induced decrease in cell viability and the increase in lactate dehydrogenase release, as well as the apoptosis rate in H9c2 cells. Schizandrin B also mitigated H/R-induced oxidative stress, as illustrated by the decrease in intracellular reactive oxygen species generation, malondialdehyde content and NADPH oxidase 2 expression, and the increase in antioxidant enzyme superoxide dismutase and glutathione peroxidase activities. In addition, Schizandrin B reversed the H/R-induced upregulation of pro-inflammatory cytokines [interleukin (IL)-1β (IL-1β) tumor necrosis factor-α, IL-6 and IL-8] and the downregulation of anti-inflammatory cytokines (transforming growth factor-β and IL-10) in the culture supernatant. Notably, Schizandrin B increased the expression of Nrf2, NAD(P)H: Quinone oxidoreductase (NQO-1) and heme oxygenase-1 (HO-1) in H/R-treated H9c2 cells, activating the Nrf2 signaling pathway. The cardioprotection of Schizandrin B against H/R injury was inhibited by Nrf2 knockdown induced byNrf-2-specific small interfering RNA (siRNA; si-Nrf2) transfection. Furthermore, Schizandrin B enhanced phosphorylated (p)-AMPK expression, while AMPK knockdown induced by AMPK-specific siRNA(si-AMPK) transfection remarkably eliminated Schizandrin B-induced cardioprotection and reduced Nrf2 expression in H/R-treated H9c2 cells. Taken together, these results suggested that Schizandrin B exerts cardioprotection on H/R injury in H9c2 cells due to its antioxidant and anti-inflammatory activities via activation of the AMPK/Nrf2 pathway.
Schizandrin protects H9c2 cells against lipopolysaccharide-induced injury by downregulating Smad3
J Biochem Mol Toxicol 2019 May;33(5):e22301.PMID:30801894DOI:10.1002/jbt.22301.
Schizandrin is a major bioactive constituent of Schisandra chinensis (Turcz.) Baill with antioxidant and anti-inflammatory properties. The objective of this study was to explore the potential effects of Schizandrin on a cell model of myocarditis. The H9c2 cells were treated with Schizandrin alone or in combination with lipopolysaccharide (LPS), after which, cell survival, migration, and the release of inflammatory cytokines were assessed. Moreover, downstream effectors and signaling pathways were studied to reveal the possible underlying mechanism. As a result, LPS stimulation induced significant cell damage as cell viability was repressed and the apoptosis was induced. In the meantime, LPS promoted the release of proinflammatory cytokines including interleukin 1β (IL-1β), IL-8, IL-6, and tumor necrosis factor (TNF-α) while repressing the release of the anti-inflammatory cytokine IL-10. Schizandrin could promote H9c2 cell migration and long-term treatment (7 days) enhanced cell viability. More interestingly, pretreatment with Schizandrin attenuated LPS-induced cell loss and inflammatory response. Besides this, Smad3 was a downstream effector of Schizandrin. The beneficial effects of Schizandrin on the H9c2 cells were attenuated when Smad3 was overexpressed. Moreover, the silencing of Smad3 deactivated c-Jun N-terminal kinase (JNK) and nuclear factor κB (NF-κB) pathways. This study preliminarily demonstrated that Schizandrin prevented LPS-induced injury in the H9c2 cells and promoted the recovery of myocardial tissues by enhancing cell viability and migration. Schizandrin conferred its beneficial effects possibly by downregulating Smad3 and inhibiting the activation of JNK and NF-κB pathways.
Schizandrin attenuates lung lesions induced by Avian pathogenic Escherichia coli in chickens
Microb Pathog 2020 Feb 11;142:104059.PMID:32058027DOI:10.1016/j.micpath.2020.104059.
Avian pathogenic Escherichia coli (APEC) can cause serious pathological changes and inflammation in chickens. Schizandrin has anti-inflammatory activity and can prevent damage to various tissues and organs. The purpose of this study was to investigate the protective effect of Schizandrin on APEC-induced lung lesions in chickens and explore the potential mechanism of Schizandrin protection. The Schizandrin (50, 100, and 200 mg/kg) was intragastrically administered for 3 days. APEC was administered using intraperitoneal (i.p.) injection to induce lung lesions. Then, chickens were sacrificed by CO2 inhalation 24 h later and the lung tissues were collected for examining histopathological changes, wet/dry (W/D) ratio, myeloperoxidase (MPO) activity, malondialdehyde (MDA), levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-8 and activation of nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways. Our findings showed that Schizandrin markedly inhibited pathological changes, pulmonary edema, MPO activity and MDA content. Moreover, Schizandrin markedly reduced the levels of TNF-α, IL-1β, IL-6 and IL-8 in lung tissue. Importantly, the mechanism responsible for these effects was attributed to the inhibitory effect of Schizandrin on NF-κB and MAPK signaling activation. In conclusion, our findings reveal that Schizandrin displays anti-oxidant and anti-inflammatory activity against APEC-induced lung lesions in chickens, paving the way for rational use of Schizandrin as a protective agent against lung-related inflammatory disease.