Schisantherin A
(Synonyms: 五味子酯甲; Gomisin-C; Schizantherin-A; Wuweizi ester-A) 目录号 : GN10368
A hepatoprotective antioxidant
Cas No.:58546-56-8
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
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Cell experiment: |
The MTT assay is performed to measure cell viability. RAW 264.7 cells are mechanically scraped, seeded in 96-well plates at 4×105 cells/mL, and incubated in a 37°C, 5% CO2 incubator overnight. After 24 h, cells, treated with 50 μL of different concentrations of Schisantherin A (0-25 mg/L) for 1 h are then stimulated with 50 μL LPS for 18 h. Subsequently, 20 μL of 5 mg/mL MTT in FBS-free medium is added to each well, and the cells are incubated for 4 h. MTT is removed and resolved with 150 μL/well DMSO. The optical density is measured at 570 nm using a microplate reader. Concentrations are determined for three wells of each sample, and this experiment done in triplicate[1]. |
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Animal experiment: |
Mice[1]Male BALB/c mice, 6-8 weeks old, are used. All mice are randomly divided into six groups: control group, Schisantherin A (40 mg/kg) group, LPS group, Schisantherin A (10, 20 and 40 mg/kg)+LPS group, and Dexamethasone (DEX)+LPS group. DEX+LPS group is used as a positive control. Schisantherin A and DEX (5 mg/kg) are conducted intraperitoneally. Mice of control and LPS groups are given an equal volume of PBS. One hour later, after slightly anesthetized with an inhalation of diethyl ether, mice are instilled intranasally (i.n.) 10 μg LPS in 50 μL PBS to induce lung injury. Control mice are given 50 μL PBS instead of LPS. All mice are alive after 7 h of LPS treatment[1]. |
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References: [1]. Ci X, et al. Schisantherin A exhibits anti-inflammatory properties by down-regulating NF-kappaB and MAPK signaling pathways in lipopolysaccharide-treated RAW 264.7 cells. Inflammation. 2010 Apr;33(2):126-36. |
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Schisantherin A is a dibenzocyclooctadiene lignan isolated from the fruit of Schisandra sphenanthera. Schisantherin A inhibits p65-NF-κB translocation into the nucleus by IκBα degradation.
The concentrations of TNF-α and IL-6 in the supernatant of cells pretreated with 2.5 or 25 mg/L of Schisantherin A are significantly decreased compared to the LPS control group (p<0.05, p<0.01). The potential cytotoxicity of Schisantherin A is evaluated by the MTT assay after incubating cells for 24 h in the absence or presence of LPS, result shows cell viabilities are not affected by the cytokines at concentrations used (0.5, 2.5, 25 mg/L). RAW 264.7 murine macrophage cells are pre-incubated with Schisantherin A for 1 h and then stimulated with 1 mg/L LPS for 12 h. Both LPS and samples are untreated in control group. After the cell culture media are collected, nitrite and PGE2 levels are determined, and Schisantherin A is found to reduce NO and PGE2 production in a dose-dependent manner[1].
Schisantherin A, a dibenzocyclooctadiene lignan isolated from the fruit of Schisandra sphenanthera, has been reported to possess varied beneficial pharmacological effects. Schisantherin A protects lipopolysaccharide-induced acute respiratory distress syndrome in mice through inhibiting NF-κB and MAPKs signaling pathways. Pretreatment with Schisantherin A markedly ameliorates LPS-induced histopathologic changes and decreases the levels of TNF-α, IL-6 and IL-1β in the BALF. In addition, the phosphorylation of NF-κB p65, IκB-α, JNK, ERK and p38 induced by LPS are suppressed by Schisantherin A. The lung wet/dry weight ratio is evaluated at 7 h after the intranasal instillation of LPS. The results show that there are no differences between control group and Schisantherin A (40 mg/kg) group (p>0.05). LPS causes a significant increase in lung wet/dry weight ratio (p<0.01) compared with the control group. Schisantherin A dose-dependently decreases the lung wet/dry weight ratio (p<0.05) compared to those in the LPS group[1].
References:
[1]. Ci X, et al. Schisantherin A exhibits anti-inflammatory properties by down-regulating NF-kappaB and MAPK signaling pathways in lipopolysaccharide-treated RAW 264.7 cells. Inflammation. 2010 Apr;33(2):126-36.
[2]. Zhou E, et al. Schisantherin A protects lipopolysaccharide-induced acute respiratory distress syndrome in mice through inhibiting NF-κB and MAPKs signaling pathways. Int Immunopharmacol. 2014 Sep;22(1):133-40.
| Cas No. | 58546-56-8 | SDF | |
| 别名 | 五味子酯甲; Gomisin-C; Schizantherin-A; Wuweizi ester-A | ||
| Canonical SMILES | CC1CC2=CC3=C(C(=C2C4=C(C(=C(C=C4C(C1(C)O)OC(=O)C5=CC=CC=C5)OC)OC)OC)OC)OCO3 | ||
| 分子式 | C30H32O9 | 分子量 | 536.57 |
| 溶解度 | ≥ 53.7mg/mL in DMSO | 储存条件 | Store at -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 | 1.8637 mL | 9.3184 mL | 18.6369 mL |
| 5 mM | 0.3727 mL | 1.8637 mL | 3.7274 mL |
| 10 mM | 0.1864 mL | 0.9318 mL | 1.8637 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。