Arnidiol
(Synonyms: 山金车二醇) 目录号 : GC35397
Arnidiol 是从Barleria Longiflora Linn F. 中提取出来的一种五环三萜烯。
Cas No.:6750-30-7
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
Arnidiol is a pentacyclic triterpene isolated from Barleria Longiflora Linn F.[1].
[1]. E Venkata Rao, et al. Anthraquinones And Arnidiol From Barleria Longiflora Linn F. India Journal of Pharmaceutical Sciences. 1999.
| Cas No. | 6750-30-7 | SDF | |
| 别名 | 山金车二醇 | ||
| Canonical SMILES | C[C@]12[C@]3([C@@](CC[C@]1([H])[C@]([C@@H]4C)([H])[C@](C)(CCC4=C)[C@@H](O)C2)([H])[C@@]5([C@@](C(C)([C@@H](O)CC5)C)([H])CC3)C)C | ||
| 分子式 | C30H50O2 | 分子量 | 442.72 |
| 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 | 2.2588 mL | 11.2938 mL | 22.5876 mL |
| 5 mM | 0.4518 mL | 2.2588 mL | 4.5175 mL |
| 10 mM | 0.2259 mL | 1.1294 mL | 2.2588 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。
Arnica montana L. - a plant of healing: review
J Pharm Pharmacol 2017 Aug;69(8):925-945.PMID:28401567DOI:10.1111/jphp.12724.
Objectives: Arnica montana is a widely used therapeutic plant used traditionally to treat various ailments. The objective of this study was to evaluate the botany, phytochemistry and ethnopharmacology along with special emphasis given on pharmacological activity of plant A. montana. Key findings: The plant extracts have been reported to possess antibacterial, antitumor, antioxidant, anti-inflammatory, antifungal and immunomodulatory activity. A wide range of chemical compounds including sesquiterpene lactones and their short-chain carbonic acid esters, flavonoids, carotenoids, essential oils, diterpenes, Arnidiol, pyrrolizidine alkaloids, coumarins, phenolic acids, lignans and oligosaccharides, etc., are found in different parts of the plant. Summary: It has been scrutinized that extensive research has been carried out to explore the therapeutic potential of flowers of the plant. Therefore, investigations should be carried out to explore the therapeutic potential of other parts of the plant for better therapeutic utilization.
ROCK1 activation-mediated mitochondrial translocation of Drp1 and cofilin are required for arnidiol-induced mitochondrial fission and apoptosis
J Exp Clin Cancer Res 2020 Feb 19;39(1):37.PMID:32075676DOI:10.1186/s13046-020-01545-7.
Background: Arnidiol is a pentacyclic triterpene diol that has multiple pharmacological activities. However, the apoptotic activities of Arnidiol in human cancer cells have not yet been explored, nor has the mechanism by which Arnidiol induces apoptosis been examined in depth. Methods: MDA-MB-231 cells and xenografted mice were treated with Arnidiol. Mitochondrial fission and apoptosis were determined by immunofluorescence, flow cytometry and related molecular biological techniques. The interaction and colocalization of cofilin and Drp1 was determined by immunoprecipitation and immunofluorescence assays. Results: Arnidiol induces mitochondrial fission and apoptosis through mitochondrial translocation of Drp1 and cofilin. Importantly, the interaction of Drp1 and cofilin in mitochondria is involved in arnidiol-induced mitochondrial fission and apoptosis. Knockdown of either Drp1 or cofilin abrogated arnidiol-induced mitochondrial translocation, interaction of Drp1 and cofilin, mitochondrial fission and apoptosis. Only dephosphorylated Drp1 (Ser637) and cofilin (Ser3) were translocated to the mitochondria. Mutants of Drp1 S637A and cofilin S3A, which mimic the dephosphorylated forms, enhanced mitochondrial fission and apoptosis induced by Arnidiol, whereas mutants of Drp1 S637D and cofilin S3E, which mimic the phosphorylated forms, suppressed mitochondrial fission and apoptosis induced by Arnidiol. A mechanistic study revealed that ROCK1 activation plays an important role in the arnidiol-mediated Drp1 and cofilin dephosphorylation and mitochondrial translocation, mitochondrial fission, and apoptosis. Conclusions: Our data reveal a novel role of both Drp1 and cofilin in the regulation of mitochondrial fission and apoptosis and suggest that Arnidiol could be developed as a potential agent for the treatment of human cancer.
Protective effects of ψ taraxasterol 3-O-myristate and Arnidiol 3-O-myristate isolated from Calendula officinalis on epithelial intestinal barrier
Fitoterapia 2016 Mar;109:230-5.PMID:26791917DOI:10.1016/j.fitote.2016.01.007.
The triterpene esters ᴪ taraxasterol-3-O-myristate (1) and arnidiol-3-O-myristate (2) were tested for their ability to protect epithelial intestinal barrier in an in vitro model. Their effects on ROS production and on trans-epithelial resistance were investigated on CaCo-2 cell monolayers both in basal and stress-induced conditions. Both compounds were able to modulate the stress damage induced by H2O2 and INFγ+TNFα, showing a potential use as model compounds for the study of new therapeutic agents for intestinal inflammations.
[Anti-inflammatory constituents from Inula japonica]
Zhongguo Zhong Yao Za Zhi 2014 Jan;39(1):83-8.PMID:24754174doi
Chemical constituents of Inula japonica were isolated and purified by repeated column chromatographies, over silica gel, and Toyopearl HW-40, and preparative HPLC. On the basis of spectral data analysis, including NMR and MS data, the structures of the isolates were elucidated and their anti-inflammatory activities were assayed. Fifteen compounds were isolated from the ethyl acetate extract of I. japonica, and their structures were elucidated as dihydrosyringenin (1), (3S, 5R, 6S, 7E)-5,6-epoxy-3-hydroxy-7-megastigmen-9-one (2), (6R, 7E) -9-hydroxy-4,7-megastigmadien-3-one (3), Arnidiol (4), taraxasterol acetate (5), 8,9,10-trihydroxythymol (6), taxifolin (7), luteolin (8), napetin (9), eupatin (10), spinacetin (11), quercetin (12), p-hydroxycinnamic acid (13), caffeic acid (14), and caffeoyl acetate (15). Compounds 1, 2, 7, 13 and 15 were isolated from the genus Inula for the first time, and compounds 3, 4, 9-11 and 14 were isolated from this plant for the first time. The anti-inflammatory activity result showed that compounds 3, 6-12 and 14 exhibited inhibition effect against leukotriene C4 (LTC4) synthesis and degranulation definitely in c-Kit Ligand (KL) induced mast cells, and compound 8 and 12 also had the suppression effect against lipopolysacharide(LPS) induced nitric oxide (NO) activity in RAW264.7 macrophages. It is firstly reported that compounds 7 and 9-11 possessed potent inhibition activities against LTC4 generation and degranulation in mast cells.
Cytotoxic and Apoptosis-inducing Activities of Taraxastane-type Triterpenoid Derivatives in Human Cancer Cell Lines
Chem Biodivers 2016 Aug;13(8):1018-29.PMID:27389784DOI:10.1002/cbdv.201500356.
Twenty-eight taraxastane-type triterpenoid derivatives 4 - 31 were prepared from the naturally occurring triterpenoids faradiol (1) and heliantriol C (3). The cytotoxic activities of these compounds and Arnidiol (2) were evaluated in leukemia (HL60), lung (A549), duodenal (AZ521), and breast (SK-BR-3) cancer cell lines. 21-Oxoarnidiol (18) and faradiol 3,16-di-O-l-alaninate (31) exhibited potent cytotoxicity, with 50% inhibitory concentrations of 0.5 - 2.7 μm. In particular, flow cytometric analysis indicated that compound 31 induced typical apoptotic cell death in HL60 cells. These results suggested that taraxastane-type triterpenoid derivatives might provide useful antitumor agents with apoptosis-inducing activity.