Dehydroeffusol
(Synonyms: 去氢厄弗酚) 目录号 : GC35834
Dehydroeffusol 是一种来自草药 Juncus effuses 的菲。Dehydroeffusol 通过选择性诱导肿瘤抑制性内质网应激和中度凋亡来抑制胃癌细胞生长和致瘤性。Dehydroeffusol 显示出非常低的毒性。
Cas No.:137319-34-7
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
Dehydroeffusol is a phenanthrene from medicinal herb Juncus effuses. Dehydroeffusol inhibits gastric cancer cell growth and tumorigenicity by selectively inducing tumor-suppressive endoplasmic reticulum stress and a moderate apoptosis. It shows very low toxicity[1][2].
Dehydroeffusol suppresses the expression of vasculogenic mimicry key gene VE-cadherin[2].Dehydroeffusol decreases the MMP2 expression and activity in gastric cancer cells[2].
[1]. Zhang B, et al. Dehydroeffusol inhibits gastric cancer cell growth and tumorigenicity by selectively inducing tumor-suppressive endoplasmic reticulum stress and a moderate apoptosis. Biochem Pharmacol. 2016 Mar 15;104:8-18. [2]. Liu W, et al. Dehydroeffusol effectively inhibits human gastric cancer cell-mediated vasculogenic mimicry with low toxicity. Toxicol Appl Pharmacol. 2015 Sep 1;287(2):98-110.
| Cas No. | 137319-34-7 | SDF | |
| 别名 | 去氢厄弗酚 | ||
| Canonical SMILES | OC1=CC=C2C3=C(C=C)C=C(O)C=C3C=CC2=C1C | ||
| 分子式 | C17H14O2 | 分子量 | 250.29 |
| 溶解度 | Soluble 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 | 3.9954 mL | 19.9768 mL | 39.9537 mL |
| 5 mM | 0.7991 mL | 3.9954 mL | 7.9907 mL |
| 10 mM | 0.3995 mL | 1.9977 mL | 3.9954 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。
Dehydroeffusol Rescues Amyloid β25-35-Induced Spatial Working Memory Deficit
Plant Foods Hum Nutr 2020 Jun;75(2):279-282.PMID:32333241DOI:10.1007/s11130-020-00816-0.
Amyloid β (Aβ) peptides produced from the amyloid precursor protein, a transmembrane protein, are neurotoxic and blocking the neurotoxicity may lead to prevention of Alzheimer's disease (AD). Here we tested whether Aβ25-35-induced cognitive decline is rescued by treatment with Dehydroeffusol, a phenanthrene isolated from Chinese medicine Juncus effusus. Dehydroeffusol (5 ~ 15 mg/kg body weight) was orally administered to mice for 6 days and Aβ25-35 (2 mM) was injected at the rate of 1 μl/min for 3 min into the lateral ventricle. Y-maze test was performed after Dehydroeffusol administration for 12 days. Aβ25-35 impaired learning and memory in the test, while the impairment was dose-dependently rescued by Dehydroeffusol administration. The present study indicates that treatment with Dehydroeffusol is effective for rescuing Aβ25-35-induced cognitive decline.
Dehydroeffusol Pprevents Amyloid β1-42-mediated Hippocampal Neurodegeneration via Reducing Intracellular Zn2+ Toxicity
Mol Neurobiol 2021 Aug;58(8):3603-3613.PMID:33770339DOI:10.1007/s12035-021-02364-3.
Dehydroeffusol, a phenanthrene isolated from Juncus effusus, is a Chinese medicine. To explore an efficacy of Dehydroeffusol administration for prevention and cure of Alzheimer's disease, here we examined the effect of Dehydroeffusol on amyloid β1-42 (Aβ1-42)-mediated hippocampal neurodegeneration. Dehydroeffusol (15 mg/kg body weight) was orally administered to mice once a day for 6 days and then human Aβ1-42 was injected intracerebroventricularly followed by oral administration for 12 days. Neurodegeneration in the dentate granule cell layer, which was determined 2 weeks after Aβ1-42 injection, was rescued by Dehydroeffusol administration. Aβ staining (uptake) was not reduced in the dentate granule cell layer by pre-administration of Dehydroeffusol for 6 days, while increase in intracellular Zn2+ induced with Aβ1-42 was reduced, suggesting that pre-administration of Dehydroeffusol prior to Aβ1-42 injection is effective for Aβ1-42-mediated neurodegeneration that was linked with intracellular Zn2+ toxicity. As a matter of fact, pre-administration of Dehydroeffusol rescued Aβ1-42-mediated neurodegeneration. Interestingly, pre-administration of Dehydroeffusol increased synthesis of metallothioneins, intracellular Zn2+-binding proteins, in the dentate granule cell layer, which can capture Zn2+ from Zn-Aβ1-42 complexes. The present study indicates that pre-administration of Dehydroeffusol protects Aβ1-42-mediated neurodegeneration in the hippocampus by reducing intracellular Zn2+ toxicity, which is linked with induced synthesis of metallothioneins. Dehydroeffusol, a novel inducer of metallothioneins, may protect Aβ1-42-induced pathogenesis in Alzheimer's disease.
Dehydroeffusol effectively inhibits human gastric cancer cell-mediated vasculogenic mimicry with low toxicity
Toxicol Appl Pharmacol 2015 Sep 1;287(2):98-110.PMID:25982451DOI:10.1016/j.taap.2015.05.003.
Accumulated data has shown that various vasculogenic tumor cells, including gastric cancer cells, are able to directly form tumor blood vessels via vasculogenic mimicry, supplying oxygen and nutrients to tumors, and facilitating progression and metastasis of malignant tumors. Therefore, tumor vasculogenic mimicry is a rational target for developing novel anticancer therapeutics. However, effective antitumor vasculogenic mimicry-targeting drugs are not clinically available. In this study, we purified 2,7-dihydroxyl-1-methyl-5-vinyl-phenanthrene, termed Dehydroeffusol, from the traditional Chinese medicinal herb Juncus effusus L., and found that Dehydroeffusol effectively inhibited gastric cancer cell-mediated vasculogenic mimicry in vitro and in vivo with very low toxicity. Dehydroeffusol significantly suppressed gastric cancer cell adhesion, migration, and invasion. Molecular mechanistic studies revealed that Dehydroeffusol markedly inhibited the expression of a vasculogenic mimicry master gene VE-cadherin and reduced adherent protein exposure on the cell surface by inhibiting gene promoter activity. In addition, Dehydroeffusol significantly decreased the expression of a key vasculogenic gene matrix metalloproteinase 2 (MMP2) in gastric cancer cells, and diminished MMP2 protease activity. Together, our results showed that Dehydroeffusol effectively inhibited gastric cancer cell-mediated vasculogenic mimicry with very low toxicity, suggesting that Dehydroeffusol is a potential drug candidate for anti-gastric cancer neovascularization and anti-gastric cancer therapy.
Dehydroeffusol inhibits hypoxia-induced epithelial-mesenchymal transition in non-small cell lung cancer cells through the inactivation of Wnt/β-catenin pathway
Biosci Rep 2020 May 29;40(5):BSR20194284.PMID:32426814DOI:10.1042/BSR20194284.
Dehydroeffusol (DHE) is a phenanthrene compound that possesses anti-tumor activity. However, the effect of DHE on non-small cell lung cancer (NSCLC) has not been investigated previously. Therefore, the objective of our study was to explore the role of DHE in NSCLC and the underlying mechanism. Our results showed that DHE significantly inhibited the cell viability of A549 cells in a dose- and time-dependent manner under normoxic condition. Moreover, A549 cells were more sensitive to DHE under hypoxic condition compared with the A549 cells cultured in normoxic condition. Hypoxia-induced increased migration and invasion abilities were mitigated by DHE in A549 cells. Treatment of DHE caused increased E-cadherin expression and decreased N-cadherin expression in hypoxia-induced A549 cells. DHE also suppressed hypoxia-induced increase in both protein and mRNA levels of hypoxia inducible factor-1α (HIF-1α) expression in A549 cells. Furthermore, DHE inhibited hypoxia-induced activation of Wnt/β-catenin pathway in A549 cells. The inhibitory effect of DHE on hypoxia-induced EMT was reversed by LiCl, which is an activator of Wnt/β-catenin signaling pathway. In conclusion, these findings demonstrated that DHE prevented hypoxia-induced EMT in NSCLC cells by inhibiting the activation of Wnt/β-catenin pathway, suggesting that DHE might serve as a therapeutic target for the NSCLC metastasis.
Dehydroeffusol inhibits viability and epithelial-mesenchymal transition through the Hedgehog and Akt/mTOR signaling pathways in neuroblastoma cells
Eur J Pharmacol 2018 Jun 15;829:93-101.PMID:29665365DOI:10.1016/j.ejphar.2018.04.012.
Neuroblastoma (NB) is the most predominant extracranial solid tumor of infancy in the world. However, current chemotherapy has limited efficacy for more advanced stages of NB due to acquired chemoresistance or acute toxicity in NB patients. Therefore, effective novel anti-NB drugs are desperately needed. The present study aimed to investigate the effects of Dehydroeffusol (DHE), a phenanthrene isolated from J. effuses, on NB cells and its underlying mechanism. The results showed that DHE treatment effectively inhibited NB cell viability in a dose-dependent manner. Moreover, DHE treatment suppressed the epithelial-mesenchymal transition (EMT) process in NB cells by promoting the expression of E-cadherin (E-cad) and restraining the expressions of N-cadherin (N-cad) and vimentin. Also, the invasive capacity and expression of MMP-2 and MMP-9 in NB cells were inhibited by DHE. Furthermore, DHE suppressed the hedgehog (Hh) and the protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathways in NB cells. In conclusion, DHE effectively inhibited the viability and EMT through inactivating the Hh and the Akt/mTOR signaling pathways in NB cells, providing a novel evidence that DHE may be a potential anti-NB drug candidate.