Tormentic acid
(Synonyms: 2Α,19Α-二羟基熊果酸) 目录号 : GC39085
A triterpene with diverse biological activities
Cas No.:13850-16-3
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
Tormentic acid is a triterpene that has been found in P. frutescens and has diverse biological activities, including anti-inflammatory, anticancer, antioxidative, and antidiabetic properties.1,2,3 It reduces hydrogen peroxide-induced increases in inducible nitric oxide synthase (iNOS) and NADPH oxidase (NOX1), as well as the production of TNF-α, IL-6, and IL-1β in rat vascular smooth muscle cells (RVSMCs) when used at concentrations of 12.5, 25, and 50 ?M.2 Tormentic acid (25 and 50 ?M) decreases hydrogen peroxide-induced generation of reactive oxygen species (ROS) in RVSMCs. It reduces ear edema induced by phorbol 12-myristate 13-acetate in mice (ID50 = 0.03 mg/ear).1 Topical application of tormentic acid (1.7 nmol) reduces the number of papillomas formed per mouse in a DMBA-TPA two-stage model of mouse skin carcinogenesis. It also reduces increases in blood glucose, insulin, and leptin levels, as well as hepatic triglyceride levels, in mice fed a high-fat diet in a model of diabetes and hyperlipidemia when administered at doses of 60 and 120 mg/kg per day.3
1.Banno, N., Akihisa, T., Tokuda, H., et al.Triterpene acids from the leaves of Perilla frutescens and their anti-inflammatory and antitumor-promoting effectsBiosci. Biotechnol. Biochem.68(1)85-90(2004) 2.Wang, Y.-L., Sun, G.-Y., Zhang, Y., et al.Tormentic acid inhibits H2O2-induced oxidative stress and inflammation in rat vascular smooth muscle cells via inhibition of the NF-κB signaling pathwayMol. Med. Rep.14(4)3559-3564(2016) 3.Wu, J.-B., Kuo, Y.-H., Lin, C.-H., et al.Tormentic acid, a major component of suspension cells of Eriobotrya japonica, suppresses high-fat diet-induced diabetes and hyperlipidemia by glucose transporter 4 and AMP-activated protein kinase phosphorylationJ. Agric. Food Chem.62(44)10717-10726(2014)
| Cas No. | 13850-16-3 | SDF | |
| 别名 | 2Α,19Α-二羟基熊果酸 | ||
| Canonical SMILES | OC([C@]12[C@]([C@](O)([C@H](C)CC2)C)([H])C3=CC[C@@]([C@@]4([C@@](C(C)([C@@H](O)[C@H](O)C4)C)([H])CC5)C)([H])[C@]5(C)[C@]3(C)CC1)=O | ||
| 分子式 | C30H48O5 | 分子量 | 488.7 |
| 溶解度 | DMSO : 50 mg/mL (102.31 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 | 2.0462 mL | 10.2312 mL | 20.4625 mL |
| 5 mM | 0.4092 mL | 2.0462 mL | 4.0925 mL |
| 10 mM | 0.2046 mL | 1.0231 mL | 2.0462 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。
The Occurrence and Biological Activity of Tormentic Acid-A Review
Molecules 2021 Jun 22;26(13):3797.PMID:34206442DOI:10.3390/molecules26133797.
This review focuses on the natural sources and pharmacological activity of Tormentic acid (TA; 2α,3β,19α-trihydroxyurs-2-en-28-oic acid). The current knowledge of its occurrence in various plant species and families is summarized. Biological activity (e.g., anti-inflammatory, antidiabetic, antihyperlipidemic, hepatoprotective, cardioprotective, neuroprotective, anti-cancer, anti-osteoarthritic, antinociceptive, antioxidative, anti-melanogenic, cytotoxic, antimicrobial, and antiparasitic) confirmed in in vitro and in vivo studies is compiled and described. Biochemical mechanisms affected by TA are indicated. Moreover, issues related to the biotechnological methods of production, effective eluents, and TA derivatives are presented.
Tormentic acid induces anticancer effects in cisplatin-resistant human cervical cancer cells mediated via cell cycle arrest, ROS production, and targeting mTOR/PI3K/AKT signalling pathway
J BUON 2020 Jan-Feb;25(1):74-79.PMID:32277616doi
Purpose: Tormentic acid has been shown to exert remarkable anti-cancer potential against different cancer cell types. In this study, the anti-cancer potential of Tormentic acid was examined in cisplatin-resistant cervical cancer cells (HeLa cells). Further, the effects of Tormentic acid on cell cycle, reactive oxygen species (ROS) production, and mTOR/PI3K/AKT signalling pathway were evaluated as well. Methods: Cell viability was evaluated by MTT assay and its impact on mTOR/PI3K/AKT signalling pathway was estimated via western blot assay. Colony formation was analysed through clonogenic assay and phase-contrast microscopy was used for the determination of apoptotic cell morphology along with DAPI staining. Fluorescence-activated cell sorting was performed for cell cycle analysis and ROS production was monitored by fluorescence microscopy. Results: The results indicated that Tormentic acid significantly supresses the proliferation of HeLa cells. These antiproliferative effects of Tormentic acid were dose-dependent. Clonogenic assay revealed anti-colony formation potential of Tormentic acid. Tormentic acid also induced remarkable morphological changes in HeLa cells, indicative of apoptosis. Further, DAPI staining assay showed formation of apoptotic bodies along with dead cells bearing apoptotic nuclei. Western blotting showed impressive increase in the expressions of pro-apoptotic proteins and decreased expression of anti-apoptotic proteins. Fluorescence-activated cell sorting (FACS) analysis revealed that Tormentic acid induced G2/M phase cell cycle arrest and its effectiveness increased with increased doses. Fluorescence intensity indicated amplified ROS production after Tormentic acid exposure. The expression of Tormentic acid on mTOR/PI3K/AKT pathway revealed blocking of this pathway with a concentration-dependent manner. Conclusions: The outcomes of the present investigation suggest that tormentic acid-induced apoptotic effects in cisplatin-resistant HeLa cells were mediated via cell cycle arrest, ROS production and targeting of mTOR/PI3K/AKT signalling pathway. Thus, Tormentic acid may be considered as a lead molecule in cancer therapeutics.
Euscaphic acid and Tormentic acid protect vascular endothelial cells against hypoxia-induced apoptosis via PI3K/AKT or ERK 1/2 signaling pathway
Life Sci 2020 Jul 1;252:117666.PMID:32298737DOI:10.1016/j.lfs.2020.117666.
Aims: Euscaphic acid and Tormentic acid are aglycones of Kaji-ichigoside F1 and Rosamultin, respectively. These four compounds are pentacyclic triterpenoid, isolated from the subterranean root of the Potentilla anserina L. Based on the protective roles against hypoxia-induced apoptosis of Euscaphic acid and Tormentic acid in vascular endothelial cells, this study was designed to determine the mechanisms. Main methods: The model of hypoxic injuries in EA. hy926 cells was established. Through applications of PI3K/AKT inhibitor, LY294002 and ERK1/2 inhibitor, PD98059, we explored the relationships between pharmacodynamic mechanisms and PI3K/AKT or ERK 1/2 signaling pathway. The anti-hypoxic effects were studied by methyl-thiazolyl-tetrazolium (MTT) assay, Hematoxylin-Eosin (HE) staining, DAPI staining, and flow cytometry. The mechanisms of anti-mitochondrial apoptosis were explored by western blot. The expressions of p-ERK 1/2, ERK 1/2, p-AKT, AKT, p-NF-κB, NF-κB, Bcl-2, Bax, Cyt C, cleaved caspase-9 and cleaved caspase-3 were detected. Key findings: Euscaphic acid protected vascular endothelial cells against hypoxia-induced apoptosis via ERK1/2 signaling pathway, and Tormentic acid brought its efficacy into full play via PI3K/AKT and ERK1/2 signaling pathways. In addition, PI3K/AKT signaling pathway positively regulated ERK1/2 pathway, and ERK1/2 pathway negatively regulated PI3K/AKT pathway. Significance: This evidence provides theoretical and experimental basis for the following research on anti-hypoxic drugs of Potentilla anserina L.
The Effects of Tormentic acid and Extracts from Callistemon citrinus on Candida albicans and Candida tropicalis Growth and Inhibition of Ergosterol Biosynthesis in Candida albicans
ScientificWorldJournal 2021 Sep 21;2021:8856147.PMID:34594161DOI:10.1155/2021/8856147.
Candida albicans and Candida tropicalis are the leading causes of human fungal infections worldwide. There is an increase in resistance of Candida pathogens to existing antifungal drugs leading to a need to find new sources of antifungal agents. Tormentic acid has been isolated from different plants including Callistemon citrinus and has been found to possess antimicrobial properties, including antifungal activity. The study aimed to determine the effects of tormentic and extracts from C. citrinus on C. albicans and C. tropicalis and a possible mode of action. The extracts and Tormentic acid were screened for antifungal activity using the broth microdilution method. The growth of both species was inhibited by the extracts, and C. albicans was more susceptible to the extract compared to C. tropicalis. The growth of C. albicans was inhibited by 80% at 100 μg/ml of both the DCM: methanol extract and the ethanol: water extract. Tormentic acid reduced the growth of C. albicans by 72% at 100 μg/ml. The effects of the extracts and Tormentic acid on ergosterol content in C. albicans were determined using a UV/Vis scanning spectrophotometer. At concentrations of Tormentic acid of 25 μg/ml, 50 μg/ml, 100 μg/ml, and 200 μg/ml, the content of ergosterol was decreased by 22%, 36%, 48%, and 78%, respectively. Similarly, the DCM: methanol extract at 100 μg/ml and 200 μg/ml decreased the content by 78% and 88%, respectively. A dose-dependent decrease in ergosterol content was observed in cells exposed to miconazole with a 25 μg/ml concentration causing a 100% decrease in ergosterol content. Therefore, Tormentic acid inhibits the synthesis of ergosterol in C. albicans. Modifications of the structure of Tormentic acid to increase its antifungal potency may be explored in further studies.
Plant-derived Tormentic acid alters the gut microbiota of the silkworm (Bombyx mori)
Sci Rep 2022 Jul 29;12(1):13005.PMID:35906393DOI:10.1038/s41598-022-17478-4.
In recent years, phytochemicals have started to attract more attention due to their contribution to health and bioactivity. Microorganisms in the intestines of organisms contribute to the processing, function, and biotransformation of these substances. The silkworm (Bombyx mori) is one of the organisms used for the biotransformation of phytochemicals due to its controlled reproduction and liability to microbial manipulation. In this study, a bioactive compound, Tormentic acid (TA), extracted from Sarcopoterium spinosum was used in the silkworm diet, and the alterations of intestinal microbiota of the silkworm were assessed. To do this, silkworms were fed on a diet with various Tormentic acid content, and 16S metagenomic analysis was performed to determine the alterations in the gut microbiota profile of these organisms. Diet with different TA content did not cause a change in the bacterial diversity of the samples. A more detailed comparison between different feeding groups indicated increased abundance of bacteria associated with health, i.e., Intestinibacter spp., Flavonifractor spp., Senegalimassilia spp., through the utilization of bioactive substances such as flavonoids. In conclusion, it might be said that using TA as a supplementary product might help ameliorate the infected gut, promote the healthy gut, and relieve the undesirable effects of medicines on the gastrointestinal system.