Dehydroabietic acid
(Synonyms: 脱氢枞酸) 目录号 : GC38407
A diterpene acid with diverse biological activities
Cas No.:1740-19-8
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
Dehydroabietic acid is a diterpene acid that has been found in P. elliottii resin and has diverse biological activities.1,2,3 It is active against L. amazonensis promastigotes (IC50 = 40 ?g/ml).1 Dehydroabietic acid (2.5, 5, and 10 ?M) increases the number of mitochondrial ridges, decreases mitochondrial outer membrane rupture, and increases the expression of FSP1 and COQ10 in an HL7720 cell model of ferroptosis induced by oleic acid .2 In vivo, dehydroabietic acid (10 and 20 mg/kg) reduces hepatic total cholesterol and triglyceride levels, ferroptosis, and lipid peroxidation in a mouse model of high-fat diet-induced non-alcoholic fatty liver disease (NAFLD). Dehydroabietic acid is also found in wood industry effluents and is considered a pollutant.3 It increases oxygen consumption and cellular heat production and reduces cellular ATP content in isolated rainbow trout (O. mykiss) hepatocytes.
1.Gon?alves, M.D., Bortoleti, B.T.S., Tomiotto-Pellissier, F., et al.Dehydroabietic acid isolated from Pinus elliottii exerts in vitro antileishmanial action by pro-oxidant effect, inducing ROS production in promastigote and downregulating Nrf2/ferritin expression in amastigote forms of Leishmania amazonensisFitoterapia128224-232(2018) 2.Gao, G., Xie, Z., Li, E.-W., et al.Dehydroabietic acid improves nonalcoholic fatty liver disease through activating the Keap1/Nrf2-ARE signaling pathway to reduce ferroptosisJ. Nat. Med.(2021) 3.Rissanen, E., Krumschnabel, G., and Nikinmaa, M.Dehydroabietic acid, a major component of wood industry effluents, interferes with cellular energetics in rainbow trout hepatocytesAquat. Toxicol.62(1)45-53(2003)
| Cas No. | 1740-19-8 | SDF | |
| 别名 | 脱氢枞酸 | ||
| Canonical SMILES | O=C([C@]1(C)CCC[C@]2(C)C3=C(CC[C@@]12[H])C=C(C(C)C)C=C3)O | ||
| 分子式 | C20H28O2 | 分子量 | 300.44 |
| 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 | 3.3285 mL | 16.6423 mL | 33.2845 mL |
| 5 mM | 0.6657 mL | 3.3285 mL | 6.6569 mL |
| 10 mM | 0.3328 mL | 1.6642 mL | 3.3285 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。
Dehydroabietic acid improves nonalcoholic fatty liver disease through activating the Keap1/Nrf2-ARE signaling pathway to reduce ferroptosis
J Nat Med 2021 Jun;75(3):540-552.PMID:33590347DOI:10.1007/s11418-021-01491-4.
The accumulation of iron-dependent lipid peroxides is one of the important causes of NAFLD. The purpose of this study is to explore the effect of Dehydroabietic acid (DA) on ferroptosis in nonalcoholic fatty liver disease (NAFLD) mice and its possible mechanisms. DA improved NAFLD and reduced triglycerides (TG), total cholesterol (TC), and lipid peroxidation level and inhibited ferroptosis in the liver of HFD-induced mice. DA binds with Keap1 to form 3 stable hydrogen bonds at VAL512 and LEU557 and increased nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response elemen (ARE) luciferase activity. DA promoted the expression downstream of Nrf2 such as heme oxygenase-1 (HO-1), glutathione (GSH) and its peroxidase 4 (GPX4), so as to eliminate the accumulation of reactive oxygen species (ROS) and reduce lipid peroxides malondialdehyde (MDA) in the liver. DA inhibited ferroptosis and increased the expression of key genes such as ferroptosis suppressor protein 1 (FSP1) in vitro and vivo. In all, DA may bind with Keap1, activate Nrf2-ARE, induce its target gene expression, inhibit ROS accumulation and lipid peroxidation, and reduce HFD-induced NAFLD.
Recent Advances on Biological Activities and Structural Modifications of Dehydroabietic acid
Toxins (Basel) 2022 Sep 12;14(9):632.PMID:36136570DOI:10.3390/toxins14090632.
Dehydroabietic acid is a tricyclic diterpenoid resin acid isolated from rosin. Dehydroabietic acid and its derivatives showed lots of medical and agricultural bioactivities, such as anticancer, antibacterial, antiviral, antiulcer, insecticidal, and herbicidal activities. This review summarized the research advances on the structural modification and total synthesis of Dehydroabietic acid and its derivatives from 2015 to 2021, and analyzed the biotransformation and structure-activity relationships in order to provide a reference for the development and utilization of Dehydroabietic acid and its derivatives as drugs and pesticides.
Effects of Dehydroabietic acid on nontarget lipidomics and proteomics of HepG2
Front Pharmacol 2022 Dec 1;13:1015240.PMID:36532744DOI:10.3389/fphar.2022.1015240.
Objective: Studies of the effects of Dehydroabietic acid on the multiomics of HepG2 hepatoma carcinoma cells are currently lacking. In this study, the molecular mechanism of the influence of Dehydroabietic acid on HepG2 cells was disclosed by studying lipidomics and proteomics. Correlations among multiomics conjoint analysis results were verified. Methods: First, proteomics analysis of HepG2 cells was carried out using Dehydroabietic acid. Differentially expressed proteins were screened and analyzed. Pathway enrichment analyses of differential proteins were compared, and the molecular mechanism was disclosed. Second, lipidomics analysis of HepG2 cells was conducted using Dehydroabietic acid. The influence of Dehydroabietic acid on HepG2 cells was determined on the lipid molecular level. Finally, a conjoint analysis of data related to differentially expressed proteins of ferroptosis and differentially changing lipid molecules was implemented. Results: A total of 260 upregulated and 961 downregulated proteins were screened in the proteomics analysis. The top five significantly enriched pathways included ferroptosis, oxidative phosphorylation, and protein processing in the endoplasmic reticulum. In the lipidomics analysis, 30 significantly differential metabolites with upregulated and downregulated expression were identified, and differentially expressed lipids were mainly related to the metabolism of glyceryl phosphatide. According to the comprehensive multiomics analysis results, real-time quantitative PCR and the enzyme-linked immunosorbent assay (ELISA), ACSL3 participated in cardiolipin metabolism. Conclusion: Dehydroabietic acid influences HepG2 cells through the above biological pathways.
Dehydroabietic acid Microencapsulation Potential as Biofilm-Mediated Infections Treatment
Pharmaceutics 2021 Jun 2;13(6):825.PMID:34199531DOI:10.3390/pharmaceutics13060825.
The antimicrobial activity of Dehydroabietic acid (DHA) for its use as an antibiofilm agent was tested in this work. DHA was assayed against a collection of Gram-positive, Gram-negative sensitive and resistant bacteria and yeasts through the minimum inhibitory concentration (MIC), MIC with Bioburden challenge, minimum bactericidal concentration (MBC), minimum biofilm inhibitory concentration (MBIC), MBIC with Bioburden challenge and growth curve studies. Toxicological studies (Artemia salina, sulforhodamine B (SRB) assay) were done to assess if the compound had antimicrobial and not cytotoxic properties. Furthermore, microencapsulation and stability studies were carried out to evaluate the chemical behavior and stability of DHA. On MIC results, Gram-positive bacteria Staphylococcus aureus ATCC 1228 and Mycobacterium smegmatis ATCC 607 presented a high efficiency (7.81 µg/mL), while on Gram-negative bacteria the highest MIC value of 125 µg/mL was obtained by all Klebsiella pneumoniae strains and Escherichia coli isolate strain HSM 303. Bioburden challenge showed that MIC, MBIC and percentage biofilm inhibition (BI) values suffered alterations, therefore, having higher concentrations. MBIC values demonstrated that DHA has a higher efficiency against S. aureus ATCC 43866 with a percentage of BI of 75.13 ± 0.82% at 0.49 µg/mL. Growth curve kinetic profiles of DHA against S. aureus ATCC 25923 were observed to be bacteriostatic. DHA-alginate beads had a average size of 2.37 ± 0.20 and 2.31 ± 0.17 × 103 µm2 with an encapsulation efficiency (EE%) around 99.49 ± 0.05%, a protection percentage (PP%) of 60.00 ± 0.05% in the gastric environment and a protection efficiency (PE%) around 88.12 ± 0.05% against UV light. In toxicological studies DHA has shown IC50 of 19.59 ± 7.40 µg/mL and a LC50 of 21.71 ± 2.18%. The obtained results indicate that DHA is a promising antimicrobial candidate against a wide range of bacteria and biofilm formation that must be further explored.
Dehydroabietic acid Is a Novel Survivin Inhibitor for Gastric Cancer
Plants (Basel) 2021 May 22;10(6):1047.PMID:34067279DOI:10.3390/plants10061047.
Gastric cancer is a malignant tumor with a high incidence and mortality rate worldwide. Nevertheless, anticancer drugs that can be used for gastric cancer treatment are limited. Therefore, it is important to develop targeted anticancer drugs for the treatment of gastric cancer. Dehydroabietic acid (DAA) is a diterpene found in tree pine. Previous studies have demonstrated that DAA inhibits gastric cancer cell proliferation by inducing apoptosis. However, we did not know how DAA inhibits the proliferation of gastric cancer cells through apoptosis. In this study, we attempted to identify the genes that induce cell cycle arrest and cell death, as well as those which are altered by DAA treatment. DAA-regulated genes were screened using RNA-Seq and differentially expressed genes (DEGs) analysis in AGS cells. RNA-Seq analysis revealed that the expression of survivin, an apoptosis inhibitor, was significantly reduced by DAA treatment. We also confirmed that DAA decreased survivin expression by RT-PCR and Western blotting analysis. In addition, the ability of DAA to inhibit survivin was compared to that of YM-155, a known survivin inhibitor. DAA was found to have a stronger inhibitory effect in comparison with YM-155. DAA also caused an increase in cleaved caspase-3, an apoptosis-activating protein. In conclusion, DAA is a potential anticancer agent for gastric cancer that inhibits survivin expression.