Euphorbia Factor L1
(Synonyms: 大戟因子L1) 目录号 : GC38165
Euphorbia factor L1, a diterpenoid isolated from Euphorbia lathyris, inhibits osteoclastogenesis and induces osteoclast apoptosis.
Cas No.:76376-43-7
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Euphorbia factor L1, a diterpenoid isolated from Euphorbia lathyris, inhibits osteoclastogenesis and induces osteoclast apoptosis.
| Cas No. | 76376-43-7 | SDF | |
| 别名 | 大戟因子L1 | ||
| Canonical SMILES | CC(O[C@]12[C@@]([C@@H](OC(CC3=CC=CC=C3)=O)[C@@H](C)C2)([H])[C@H]([C@]4(CC[C@H](C5(C)C)[C@H]5/C=C(C)\C1=O)CO4)OC(C)=O)=O | ||
| 分子式 | C32H40O8 | 分子量 | 552.66 |
| 溶解度 | Soluble in DMSO | 储存条件 | 4°C, protect from light |
| 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 | 1.8094 mL | 9.0472 mL | 18.0943 mL |
| 5 mM | 0.3619 mL | 1.8094 mL | 3.6189 mL |
| 10 mM | 0.1809 mL | 0.9047 mL | 1.8094 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。
Effect of Euphorbia Factor L1 on oxidative stress, apoptosis, and autophagy in human gastric epithelial cells
Phytomedicine 2019 Nov;64:152929.PMID:31454650DOI:10.1016/j.phymed.2019.152929.
Background: Euphorbia Factor L1 (EFL1), a lathyrane-type diterpenoid from the medicinal herb Euphorbia lathyris L. (Euphorbiaceae), has been reported for many decades to induce gastric irritation, but the underlying mechanisms remain unclear. Purpose: The objective of this study was to investigate EFL1-induced cytotoxicity and the potential mechanisms of action on the human normal gastric epithelial cell GES-1. Methods: GES-1 cells were treated with EFL1 (12.5-200 μM) for different time intervals, and cell survival, LDH release, intracellular reactive oxygen species (ROS), malondialdehyde (MDA) content, and superoxide dismutase (SOD) activity were detected. Mitochondrial membrane potential (MMP) assay, DAPI staining, DNA fragment assay, and annexin V-FITC/PI staining were performed. The interaction between EFL1 and Bcl-2, cytochrome c, caspase-9, caspase-3, PI3K, AKT, and mTOR proteins was simulated by molecular docking. The mRNA and protein expression of apoptosis and autophagy factors were detected by RT-qPCR and Western blotting. Results: EFL1 decreased survival, increased LDH leakage, and induced abnormal production of ROS, MDA and SOD in GES-1 cells. Mitochondria-mediated apoptosis was characterized by decreased MMP, condensed nuclei, fragmented DNA, and increased apoptosis rate. EFL1 interacted with proteins via hydrogen bonding. The mRNA, total or phosphorylated protein expression of Bcl-2, mitochondrial cytochrome c, PI3K, AKT, mTOR and p62 were downregulated; in contrast, those of cytoplasmic cytochrome c, cleaved caspase-9, cleaved caspase-3, LC3-ll and Beclin-1 were upregulated. Conclusion: These findings indicated that EFL1 decreased the survival of GES-1 cells through EFL1-induced oxidative stress, activation of the mitochondria-mediated apoptosis as well as autophagy via inhibition of the PI3K/AKT/mTOR pathway.
Euphorbia Factor L1 inhibits osteoclastogenesis by regulating cellular redox status and induces Fas-mediated apoptosis in osteoclast
Free Radic Biol Med 2017 Nov;112:191-199.PMID:28774817DOI:10.1016/j.freeradbiomed.2017.07.030.
Excessive bone resorption caused by increased osteoclast number or activity leads to a variety of bone diseases including osteoporosis, rheumatoid arthritis and periodontitis. Thus, the therapeutic strategy for these diseases has been focused primarily on the inhibition of osteoclast formation and function. This study shows that Euphorbia Factor L1 (EFL1), a diterpenoid isolated from Euphorbia lathyris, inhibited osteoclastogenesis and induced osteoclast apoptosis. EFL1 suppressed osteoclast formation and bone resorption at both initial and terminal differentiation stages. EFL1 inhibited receptor activator of NF-κB ligand (RANKL)-induced NFATc1 induction with attenuated NF-κB activation and c-Fos expression. EFL1 decreased the level of reactive oxygen species by scavenging them or activating Nrf2, and inhibited PGC-1β that regulates mitochondria biogenesis. In addition, EFL1 induced apoptosis in differentiated osteoclasts by increasing Fas ligand expression followed by caspase activation. Moreover, EFL1 inhibited inflammation-induced bone erosion and ovariectomy-induced bone loss in mice. These findings suggest that EFL1 inhibits osteoclast differentiation by regulating cellular redox status and induces Fas-mediated apoptosis in osteoclast, and may provide therapeutic potential for preventing or treating bone-related diseases caused by excessive osteoclast.
Euphorbia Factor L1 reverses ABCB1-mediated multidrug resistance involving interaction with ABCB1 independent of ABCB1 downregualtion
J Cell Biochem 2011 Apr;112(4):1076-83.PMID:21308736DOI:10.1002/jcb.23021.
Euphorbia Factor L1 (EFL1) belongs to diterpenoids of genus Euphorbia. In this article, its reversal activity against ABCB1-mediated MDR in KBv200 and MCF-7/adr cells was reported. However, EFL1 did not alter the sensitivity of KB and MCF-7 cells to chemotherapeutic agents. Meanwhile, EFL1 significantly increased accumulation of doxorubicin and rhodamine 123 in KBv200 and MCF-7/adr cells, showing no significant influence on that of KB and MCF-7 cells. Furthermore, EFL1 could enhance the ATP hydrolysis activity of ABCB1 stimulated by verapamil. At the same time, EFL1 inhibited the efflux of ABCB1 in KBv200 and MCF-7/adr cells. In addition, EFL1 did not downregulate expression of ABCB1 in KBv200 and MCF-7/adr cells either in mRNA or protein level.
Effect of Euphorbia Factor L1 on intestinal barrier impairment and defecation dysfunction in Caenorhabditis elegans
Phytomedicine 2019 Dec;65:153102.PMID:31654989DOI:10.1016/j.phymed.2019.153102.
Background: Euphorbia Factor L1 (EFL1) is a lathyrane-type diterpenoid from the medicinal herb Euphorbia lathyris L., and has been reported with intestinal toxicity, but the potential mechanisms remain unknown. Purpose: The objective of this study was to investigate the intestinal toxicity of EFL1 and the underlying mechanisms using nematode Caenorhabditis elegans. Methods: C. elegans were exposed to 0-200 μM EFL1 for 72 h, then the survival rate, body length and body width, locomotion and chemoreception behavior, intestinal ROS and lipofuscin accumulation, intestinal permeability, and defecation rhythm were detected. The γ-aminobutyric acid（GABA) energic neurons AVL and DVB were shown via green fluorescent protein under a laser scanning confocal microscope. The structure of GABA transporter UNC-47 were predicted by homology modeling, and the interaction between EFL1 and UNC-47 was simulated by molecular docking. The mRNA expression of genes related to oxidative stress, intestinal permeability and defecation after EFL1 exposure were detected by RT-qPCR. Results: EFL1 did not induce lethality of nematodes. The general toxicity was characterized by abnormal growth, locomotion and chemoreception. The intestinal barrier was leaky, due to down-regulated cell junction and active cation transport. The mean defecation cycle length in nematodes was decreased, relating to disorder vesicular and ion transport, enhanced rhythm behavior and muscle contraction. The dysfunctional defecation also attributed to injured UNC-47 protein, as well as GABAergic neurons AVL and DVB. Excessive ROS and lipofuscin accumulation were observed in intestine, along with activation of antioxidant enzymes of SOD, COQ7 and CAT. Conclusion: This study elucidated the EFL1-induced intestinal toxicity in nematodes, characterized as leaky intestinal barrier and accelerated defecation behavior. The underlying mechanisms were involved in oxidative stress, cell junctions, transportation, rhythm behavior, muscle contraction, and GABAergic neurons.
Microbial and chemical transformations of Euphorbia Factor L1 and the P-glycoprotein inhibitory activity in zebrafishes
Nat Prod Res 2023 Mar;37(6):871-881.PMID:35776104DOI:10.1080/14786419.2022.2095379.
Euphorbia Factor L1 (EFL1, 1) is a natural tri-ester of 6,17-epoxylathyrol with cancer multidrug resistance (MDR) reversal activity. Several EFL1 derivatives (2-9) were prepared by chemical and microbial transformations and their ability to inhibit P-glycoprotein (P-gp) activity was estimated. Six de-acylated derivatives (2-7) were obtained through base-hydrolysis of 1, and the base-catalysed hydrolysis via KOH and NaOH yielded different hydrolysed products of 1. Two biotransformed products (8-9) were directly obtained via microbial transformation of 1, and 8 was also formed by microbial conversion of the hydrolysed product 3. The P-gp modulation of 1-9 was assessed by a zebrafish model. The substrate 1 and its biotransformed product 9 as the tri-esters of lathyranes possessed the highest P-gp inhibitory activity with IC50 values of 34.97 and 15.50 µM, respectively, through down-regulating P-gp expression at the protein level rather than at MDR1 mRNA level.