Eclalbasaponin I
(Synonyms: 墨旱莲皂苷I) 目录号 : GC65123
Eclalbasaponin I 从 Eclipta prostrata L. (Asteraceae) 分离，具有抗肿瘤活性。 Eclalbasaponin I 抑制肝癌细胞 smmc-7721 的增殖，其 IC50 值为 111.1703 μg/ml。
Cas No.:158511-59-2
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
Eclalbasaponin I is isolated from Eclipta prostrata L with antitumor activity. Eclalbasaponin I inhibits the proliferation of hepatoma cell smmc-7721 with an IC50 value of 111.1703 μg/ml[1].
[1]. Liu QM, et al. Eclipta prostrata L. phytochemicals: isolation, structure elucidation, and their antitumor activity. Food Chem Toxicol. 2012 Nov;50(11):4016-22.
| Cas No. | 158511-59-2 | SDF | Download SDF |
| 别名 | 墨旱莲皂苷I | ||
| 分子式 | C42H68O14 | 分子量 | 796.98 |
| 溶解度 | DMSO : 100 mg/mL (125.47 mM; Need ultrasonic) | 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 | 1.2547 mL | 6.2737 mL | 12.5474 mL |
| 5 mM | 0.2509 mL | 1.2547 mL | 2.5095 mL |
| 10 mM | 0.1255 mL | 0.6274 mL | 1.2547 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。
Eclalbasaponin I causes mitophagy to repress oxidative stress-induced apoptosis via activation of p38 and ERK in SH-SY5Y cells
Free Radic Res 2019 Jun;53(6):655-668.PMID:31185752DOI:10.1080/10715762.2019.1620937.
Oxidative stress accompanying excessive accumulation of reactive oxygen species (ROS) and mitochondrial dysfunction leads to the occurrence of neurodegenerative diseases. Our previous study showed that Eclalbasaponin I (EcI), a triterpene saponin isolated from Aralia elata (Miq.) Seem. (A. elata), repressed oxidative stress in human neuroblastoma SH-SY5Y cells. However, the detailed mechanism remains unclear. In this study, pretreatment with EcI in SH-SY5Y cells significantly activated the p38-mitogenactivated protein kinase (p38), the extracellular regulated protein kinase (ERK), whereas it did not affect the c-jun NH2 terminal kinases (JNK). In accordance with the initial findings, EcI-induced neuroprotective effect was attenuated by SB203580 (SB, a p38 inhibitor) or FR180204 (FR, an ERK inhibitor), being further confirmed by specific small interfering RNA (siRNA). Inhibition of either p38 or ERK up-regulated the apoptosis induction in EcI- and H2O2-cotreated cells. Furthermore, p38 or ERK suppression enhanced intracellular and mitochondrial ROS generation, decreased the activities of endogenous antioxidant defences as well as the mitochondrial membrane potential (MMP), resulting in dysfunction of mitochondria. In addition, EcI-induced autophagy and mitophagy were obviously down-regulated when p38 or ERK activation was blocked. Cumulatively, these findings supported that EcI-caused mitophagy contributed to the neuroprotective effect through p38 or ERK activation. Mitophagy induction might be an effective therapeutic intervention in neurodegenerative diseases.
Eclalbasaponin I from Aralia elata (Miq.) Seem. reduces oxidative stress-induced neural cell death by autophagy activation
Biomed Pharmacother 2018 Jan;97:152-161.PMID:29091860DOI:10.1016/j.biopha.2017.10.106.
Oxidative stress has been proposed to contribute to DNA damage and is involved in many neurodegenerative diseases. It has been reported that Aralia elata (Miq.) Seem. (A. elata) exhibits an anti-oxidative effect but the mechanisms underlying this protective effect are still unclear. In this study, six known triterpene saponins were isolated from the buds of A. elata, a well-known medicinal and edible plant in Northeast China. Subsequently, the anti-oxidative effects of all six triterpene saponins were screened by H2O2-induced damage in human neuronblastoma SH-SY5Y cells. Compound 6, also known as Eclalbasaponin I (EcI), was the most potent. Furthermore, the mechanism by which EcI combats H2O2-induced oxidative stress was investigated. The data suggested that EcI could down-regulate apoptosis induction and the generation of reactive oxygen species (ROS) induced by 200μM H2O2 in SH-SY5Y cells. Moreover, EcI increased the activities of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxides (GSH-Px), reduced the levels of malondialdehyde (MDA) to restore the antioxidant defense system, and activated the nuclear factor E2-related factor (Nrf2)/heme oxygenase 1 (HO-1) pathway to combat oxidative stress. In addition, EcI also promoted autophagy during this process. Interestingly, the protective effect was remarkably reversed by autophagy inhibitors, bafilomycin A1 (Baf) or 3-Methyladenine (3-MA). These results demonstrate that autophagy is contribute to the protective effect of EcI. Collectively, our findings provide a new insight into the potential protective effect of EcI by focusing on the role of autophagy.
Eclalbasaponin II induces autophagic and apoptotic cell death in human ovarian cancer cells
J Pharmacol Sci 2016 Sep;132(1):6-14.PMID:27032907DOI:10.1016/j.jphs.2016.02.006.
Triterpenoids echinocystic acid and its glycosides, isolated from several Eclipta prostrata, have been reported to possess various biological activities such as anti-inflammatory, anti-bacterial, and anti-diabetic activity. However, the cytotoxicity of the triterpenoids in human cancer cells and their molecular mechanism of action are poorly understood. In the present study, we found that eclalbasaponin II with one glucose moiety has potent cytotoxicity in three ovarian cancer cells and two endometrial cancer cells compared to an aglycone echinocystic acid and Eclalbasaponin I with two glucose moiety. Eclalbasaponin II treatment dose-dependently increased sub G1 population. Annexin V staining revealed that eclalbasaponin II induced apoptosis in SKOV3 and A2780 ovarian cancer cells. In addition, eclalbasaponin II-induced cell death was associated with characteristics of autophagy; an increase in acidic vesicular organelle content and elevation of the levels of LC3-II. Interestingly, autophagy inhibitor BaF1 suppressed the eclalbasaponin II-induced apoptosis. Moreover, eclalbasaponin II activated JNK and p38 signaling and inhibited the mTOR signaling. We further demonstrated that pre-treatment with a JNK and p38 inhibitor and mTOR activator attenuated the eclalbasaponin II-induced autophagy. This suggests that eclalbasaponin II induces apoptotic and autophagic cell death through the regulation of JNK, p38, and mTOR signaling in human ovarian cancer cells.
Antiproliferative activity of triterpenoids from Eclipta prostrata on hepatic stellate cells
Phytomedicine 2008 Sep;15(9):775-80.PMID:18061418DOI:10.1016/j.phymed.2007.10.004.
Hepatic stellate cells (HSCs) have been known to play a key role in the pathogenesis of liver fibrosis. In the course of screening antifibrotic activity of natural products employing HSC-T6, a rat hepatic stellate cell line as an in vitro assay system, the methanolic extract of aerial parts of Eclipta prostrata L. showed significant inhibitory activity on HSCs proliferation. Activity-guided fractionation led to the isolation of five oleanane-type triterpenoids, echinocystic acid (1), eclalbasaponin II (2), eclalbasaponin V (3), Eclalbasaponin I (4) and eclalbasaponin III (5), which are all echinocystic acid derivatives. Among the five echinocystic acid derivatives isolated, echinocystic acid (1) and eclalbasaponin II (2) significantly inhibited the proliferation of HSCs in dose- and time-dependent manners. Our present study also suggests the importance of free carboxylic acid at C-28 position in echinocystic acid derivatives for the antifibrotic activity. Taken together, antifibrotic activity of E. prostrata and its triterpenoids might suggest the therapeutic potentials against liver fibrosis.
Eclipta prostrata L. phytochemicals: isolation, structure elucidation, and their antitumor activity
Food Chem Toxicol 2012 Nov;50(11):4016-22.PMID:22902823DOI:10.1016/j.fct.2012.08.007.
Eclipta prostrata L., (Asteraceae), is used in China for both food and medicine purposes. This research is concerned with the isolation and purification of phytochemical constituents from the aerial parts of E. prostrata, using gradient solvent fractionation, macroporous resin, silica gel, Sephadex LH-20 and ODS columns, and TLC analyses. Four fractions (water, 30% ethanol, 60% ethanol and 90% ethanol) were obtained. Four compounds, wedelolactone (I), Eclalbasaponin I (II), luteolin (III) and luteolin-7-O-glucoside (IV) were purified and their structures were identified by the interpretation of spectroscopic analyses including MS, (1)H and (13)C NMR. Antitumor activities of extracts (total fraction), four fractions and the isolated compounds were assessed using hepatoma cell smmc-7721 as an in vitro assay system. The 30% ethanol fraction and Eclalbasaponin I dose-dependently inhibited the proliferation of hepatoma cell smmc-7721 with IC(50) values of 74.2399 and 111.1703 μg/ml, respectively, more strongly compared with 5-fluorouracil positive control group with the IC(50) value of 195.3131 μg/ml. Antitumor activities of other fractions and compounds were lower than positive control. These results suggested that some specific compounds or extracts from E. prostrata are potential sources of natural anti-tumor materials and worthy of further study.