Schisantherin A is a dibenzocyclooctadiene lignan. 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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

536.57

C₃₀H₃₂O₉

58546-56-8

五味子酯甲

Room temperature in continental US; may vary elsewhere.

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

In Vitro: 

DMSO : ≥ 100 mg/mL (186.37 mM)

* “≥” means soluble, but saturation unknown.

*

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, 6 months; -20°C, 1 month。-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。

In Vivo:

请根据您的实验动物和给药方式选择适当的溶解方案。以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：

——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用； 以下溶剂前显示的百
分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

• 1.

  请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% saline

  Solubility: ≥ 2.5 mg/mL (4.66 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (4.66 mM，饱和度未知) 的澄清溶液。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；向上述体系中加入50 μL Tween-80，混合均匀；然后继续加入 450 μL生理盐水定容至 1 mL。

  将 0.9 g 氯化钠，完全溶解于 100 mL ddH₂O 中，得到澄清透明的生理盐水溶液

• 2.

  请依序添加每种溶剂： 10% DMSO    90% corn oil

  Solubility: ≥ 2.5 mg/mL (4.66 mM); Clear solution

  此方案可获得 ≥ 2.5 mg/mL (4.66 mM，饱和度未知) 的澄清溶液，此方案不适用于实验周期在半个月以上的实验。

  以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL玉米油中，混合均匀。

• [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.

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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

• [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.