Ethyl 3,4-dihydroxybenzoate
(Synonyms: 3,4-二羟基苯甲酸乙酯,Ethyl protocatechuate) 目录号 : GC61669
Ethyl3,4-dihydroxybenzoate(Ethylprotocatechuate)是一种抗氧化剂，是一种在花生种子的种皮中发现的脯氨酰羟化酶(prolyl-hydroxylase)抑制剂。Ethyl3,4-dihydroxybenzoate通过激活NO合酶(NOsynthase)并产生线粒体ROS来保护心肌。Ethyl3,4-dihydroxybenzoate可诱导ESCC细胞自噬(autophagy)和凋亡(apoptosis)。Ethyl3,4-dihydroxybenzoate是胶原蛋白合成抑制剂，具有骨骼保护作用。
Cas No.:3943-89-3
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Ethyl 3,4-dihydroxybenzoate (Ethyl protocatechuate), an antioxidant, is a prolyl-hydroxylase inhibitor found in the testa of peanut seeds. Ethyl 3,4-dihydroxybenzoate protects myocardium by activating NO synthase and generating mitochondrial ROS. Ethyl 3,4-dihydroxybenzoate induces cell autophagy and apoptosis in ESCC cells. Ethyl 3,4-dihydroxybenzoate is a collagen synthesis inhibitor and has a bone protecting-effect[1][2][3][4].
[1]. Bo Han, et al. A prolyl-hydroxylase inhibitor, ethyl-3,4-dihydroxybenzoate, induces cell autophagy and apoptosis in esophageal squamous cell carcinoma cells via up-regulation of BNIP3 and N-myc downstream-regulated gene-1. PLoS One. 2014 Sep 18;9(9):e107204. [2]. Sebastian Philipp, et al. Desferoxamine and ethyl-3,4-dihydroxybenzoate protect myocardium by activating NOS and generating mitochondrial ROS. Am J Physiol Heart Circ Physiol. 2006 Jan;290(1):H450-7. [3]. Byeong-Ju Kwon, et al. Ethyl-3,4-dihydroxybenzoate with a dual function of induction of osteogenic differentiation and inhibition of osteoclast differentiation for bone tissue engineering. Tissue Eng Part A. 2014 Nov;20(21-22):2975-84. [4]. D Nandan, et al. Ethyl-3,4-dihydroxybenzoate inhibits myoblast differentiation: evidence for an essential role of collagen. J Cell Biol. 1990 May;110(5):1673-9.
| Cas No. | 3943-89-3 | SDF | |
| 别名 | 3,4-二羟基苯甲酸乙酯,Ethyl protocatechuate | ||
| Canonical SMILES | O=C(OCC)C1=CC=C(O)C(O)=C1 | ||
| 分子式 | C9H10O4 | 分子量 | 182.18 |
| 溶解度 | DMSO : 100 mg/mL (548.91 mM; Need ultrasonic) | 储存条件 | 4°C, stored under nitrogen |
| 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 | 5.4891 mL | 27.4454 mL | 54.8908 mL |
| 5 mM | 1.0978 mL | 5.4891 mL | 10.9782 mL |
| 10 mM | 0.5489 mL | 2.7445 mL | 5.4891 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。
Phenolic Compound Ethyl 3,4-dihydroxybenzoate Retards Drug Efflux and Potentiates Antibiotic Activity
Antibiotics (Basel) 2022 Apr 8;11(4):497.PMID:35453250DOI:10.3390/antibiotics11040497.
The World Health Organization indicated that antibiotic resistance is one of the greatest threats to health, food security, and development in the world. Drug resistance efflux pumps are essential for antibiotic resistance in bacteria. Here, we evaluated the plant phenolic compound Ethyl 3,4-dihydroxybenzoate (EDHB) for its efflux pump inhibitory (EPI) activity against drug-resistant Escherichia coli. The half-maximal inhibitory concentration, modulation assays, and time-kill studies indicated that EDHB has limited antibacterial activity but can potentiate the activity of antibiotics for drug-resistant E. coli. Dye accumulation/efflux and MALDI-TOF studies showed that EDHB not only significantly increases dye accumulation and reduces dye efflux but also increases the extracellular amount of antibiotics in the drug-resistant E. coli, indicating its interference with substrate translocation via a bacterial efflux pump. Molecular docking analysis using AutoDock Vina indicated that EDHB putatively posed within the distal binding pocket of AcrB and in close interaction with the residues by H-bonds and hydrophobic contacts. Additionally, EDHB showed an elevated postantibiotic effect on drug-resistant E. coli. Our toxicity assays showed that EDHB did not change the bacterial membrane permeability and exhibited mild human cell toxicity. In summary, these findings indicate that EDHB could serve as a potential EPI for drug-resistant E. coli.
Ethyl 3,4-dihydroxybenzoate (EDHB): a prolyl hydroxylase inhibitor attenuates acute hypobaric hypoxia mediated vascular leakage in brain
J Physiol Sci 2016 Jul;66(4):315-26.PMID:26649730DOI:10.1007/s12576-015-0429-9.
Sudden exposure to altitude hypoxia is responsible for acute mountain sickness (AMS) in un-acclimatized persons. If not treated in time, AMS can worsen and leads to high altitude cerebral edema, which can be fatal. Present study explores the efficacy of Ethyl 3,4-dihydroxybenzoate (EDHB), a prolyl hydroxylase enzyme inhibitor, in modulating adaptive responses to hypobaric hypoxia (HH) in rat brain. Male Sprague-Dawley rats treated with EDHB (75 mg/kg for 3 days), were subjected to acute HH exposure at 9144 m (30,000 ft) for 5 h. Animals were assessed for transvascular leakage and edema formation in brain and role of key inflammatory markers along with hypoxia responsive genes. HH stress increased transvascular permeability and edema formation in conjunction with upregulation of nuclear factor-κB (NF-κB) and its regulated proteins. There was surge in pro-inflammatory cytokines tumor necrosis factor-α, interleukin-6, interferon-γ, monocyte chemoattractant protein-1 and decrement in anti-inflammatory cytokine interleukin-10. Further, upregulation of vascular endothelial growth factor (VEGF), a vascular permeability marker and down-regulation of antioxidant and anti-inflammatory proteins hemoxygenase (HO-1) and metallothionein (MT-1) was also observed under hypoxia. EDHB supplementation effectively scaled down HH induced cerebral edema with concomitant downregulation of brain NF-κB expression. There was significant curtailment of pro-inflammatory cytokines and cell adhesion molecules. There was significant downregulation of permeability factor VEGF by EDHB with concomitant increment in hypoxia inducible factor (HIF1α) and anti-inflammatory proteins HO-1 and MT-1 compared to HH control thus accentuating the potential of EDHB as effective hypoxic preconditioning agent in ameliorating HH mediated injury in brain.
Preconditioning with Ethyl 3,4-dihydroxybenzoate augments aerobic respiration in rat skeletal muscle
Hypoxia (Auckl) 2016 May 13;4:109-120.PMID:27800513DOI:10.2147/HP.S102943.
Muscle respiratory capacity decides the amount of exertion one's skeletal muscle can undergo, and endurance exercise is believed to increase it. There are also certain preconditioning methods by which muscle respiratory and exercise performance can be enhanced. In this study, preconditioning with Ethyl 3,4-dihydroxybenzoate (EDHB), a prolyl hydroxylase domain enzyme inhibitor, has been investigated to determine its effect on aerobic metabolism and bioenergetics in skeletal muscle, thus facilitating boost in physical performance in a rat model. We observed that EDHB supplementation increases aerobic metabolism via upregulation of HIF-mediated GLUT1 and GLUT4, thus enhancing glucose uptake in muscles. There was also a twofold rise in the activity of enzymes of tricarboxylic acid (TCA) cycle and glycolysis, ie, hexokinase and phosphofructokinase. There was an increase in citrate synthase and succinate dehydrogenase activity, resulting in the rise in the levels of ATP due to enhanced Krebs cycle activity as substantiated by enhanced acetyl-CoA levels in EDHB-treated rats as compared to control group. Increased lactate dehydrogenase activity, reduced expression of monocarboxylate transporter 1, and increase in monocarboxylate transporter 4 suggest transport of lactate from muscle to blood. There was a concomitant decrease in plasma lactate, which might be due to enhanced transport of lactate from blood to the liver. This was further supported by the rise in liver pyruvate levels and liver glycogen levels in EDHB-supplemented rats as compared to control rats. These results suggest that EDHB supplementation leads to improved physical performance due to the escalation of aerobic respiration quotient, ie, enhanced muscle respiratory capacity.
Inhibition of prolyl hydroxylation during collagen biosynthesis in human skin fibroblast cultures by Ethyl 3,4-dihydroxybenzoate
J Invest Dermatol 1987 Oct;89(4):405-9.PMID:2822818DOI:10.1111/1523-1747.ep12471775.
The enzymatically catalyzed formation of 4-hydroxyproline plays a key role in the intracellular biosynthesis of collagen, since a critical number of 4-hydroxyprolyl residues is required for synthesis and secretion of triple-helical procollagen molecules under physiologic conditions. The enzyme catalyzing the conversion of prolyl residues to 4-hydroxyproline, prolyl 4-hydroxylase, requires ferrous ion, alpha-ketoglutarate, and ascorbate for its activity. 3,4-Dihydroxybenzoic acid has been known to act as potent competitive inhibitor of purified prolyl 4-hydroxylase with respect to one or several of the cofactors or cosubstrates of the enzyme. 3,4-Dihydroxybenzoic acid, however, is a poor inhibitor of prolyl hydroxylation in intact cells, probably due to its polarity not allowing it to enter the cells. In this study, several hydrophobic modifications of 3,4-dihydroxybenzoic acid were tested in human skin fibroblast cultures for their efficacy to inhibit the synthesis of 4-hydroxyproline. The results indicated that the ethyl ester of 3,4-dihydroxybenzoic acid was an efficient inhibitor of prolyl hydroxylation in fibroblast cultures, with Ki of approximately 0.4 mM. Ethyl 3,4-dihydroxybenzoate had little, if any, effect on the hydroxylation of lysyl residues, and it did not affect total protein synthesis or DNA replication in these cells. To test the hypothesis that Ethyl 3,4-dihydroxybenzoate might serve as a potential antifibrotic agent, its efficacy in inhibiting prolyl hydroxylation in scleroderma fibroblasts was also tested. The results indicated that the synthesis of 4-hydroxyproline in scleroderma cell cultures was similarly reduced by Ethyl 3,4-dihydroxybenzoate. Thus, structural analogs of the cofactors or cosubstrates of prolyl 4-hydroxylase, such as Ethyl 3,4-dihydroxybenzoate tested here or its further modifications, may serve as inhibitors of posttranslational hydroxylation of prolyl residues also in vivo. These compounds could potentially provide a novel means of reducing collagen deposition in tissues in fibrotic diseases, such as scleroderma.
Urinary parabens and their derivatives associated with oxidative stress biomarkers in children from South and Central China: Repeated measures
Sci Total Environ 2022 Apr 15;817:152639.PMID:34971688DOI:10.1016/j.scitotenv.2021.152639.
Previous studies implied that elevated exposure to parabens may result in increased oxidative stress. However, the association between exposure to paraben derivatives and oxidative stress biomarkers in children has been rarely studied. This study examined the associations between exposure to paraben derivatives and oxidative stress biomarkers in Chinese children. Nine targeted compounds of parabens and their derivatives including methyl paraben (MeP), ethyl paraben (EtP), propyl paraben (PrP), butyl paraben (BuP), p-hydrox4ybenzoic acid (p-HB), 3,4-dihydroxy benzoic acid (3,4-DHB), benzoic acid, methyl 3,4-dihydroxybenzoate (rOH-MeP), and Ethyl 3,4-dihydroxybenzoate (rOH-EtP) were detected in urine collected from 139 children from South and Central China. Additionally, 8-hydroxy-2'-deoxyguanosine (8-OHdG), 8-hydroxyguanosine (8-OHG), and 4-hydroxy-2-nonenal mercapturic acid (HNE-MA) were measured as oxidative stress biomarkers. All targeted compounds (except for BuP) were frequently detected in urine (detection frequencies ranged 80.8%-100%). Linear mixed effects model revealed that all targeted compounds (with detection frequencies >50%), except for EtP, were significantly associated with an increase in 8-OHdG. rOH-EtP was found to be significantly associated with 8-OHG (β = 0.12; 95% confidence interval [95% CI]: 0.08, 0.16) positively. In addition, PrP and benzoic acid were associated with elevated levels of HNE-MA. Weighted quantile sum regression revealed that co-exposure to the targeted compounds was positively associated with 8-OHdG (β = 0.17; 95% CI: 0.12, 0.22), 8-OHG (β = 0.14; 95% CI: 0.10, 0.18), and HNE-MA (β = 0.43; 95% CI: 0.27, 0.59); rOH-EtP and benzoic acid were the major contributors for the combined effects on oxidative stress of nucleic acids and lipid, respectively. Our findings provide new evidence for the effects of exposure to paraben derivatives on nucleic acid oxidative damage and lipid peroxidation in children.