Veratric acid
(Synonyms: 藜芦酸) 目录号 : GC61371
Veratricacid(3,4-Dimethoxybenzoicacid)是从蔬菜和水果中得到的多酚物质，可口服，具有抗氧化、保护心血管和抗炎活性。当细胞受到UVB辐射时，Veratricacid能够减少上调的COX-2表达，降低PGE2和IL-6水平。
Cas No.:1993-7-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Veratric acid (3,4-Dimethoxybenzoic acid) is an orally active phenolic compound derived from vegetables and fruits, has antioxidant[1] and anti-inflammatory activities[3]. Veratric acid also acts as a protective agent against hypertension-associated cardiovascular remodelling[2]. Veratric acid reduces upregulated COX-2 expression, and levels of PGE2, IL-6 after UVB irradiation[3].
Veratric acid (100, 200 μM) suppresses iNOS expression in LPS-stimulated RAW264.7 cells. Veratric acid (200 μM) inhibits LPS-induced activation of the PI3K/Akt pathway, HAT activation and HDAC3 expression in RAW264.7 cells[1].Veratric Acid (10-100 μg/mL) has anti-inflammatory activity, protects HaCaT cells against UVB-mediated phototoxicity, increases S-phase cells, and prevents UVB-mediated apoptosis[3]. Veratric acid reduces upregulated COX-2 expression, and levels of PGE2, IL-6 after UVB irradiation[3].
Veratric acid (40 mg/kg, p.o., b.w.) significantly promotes ventricular function, reduces lipid peroxidation and increases antioxidants in l-NAME-induced hypertensive rats[2].
[1]. Choi WS, et al. Veratric acid inhibits iNOS expression through the regulation of PI3K activation and histone acetylation in LPS-stimulated RAW264.7 cells. Int J Mol Med. 2015 Jan;35(1):202-10. [2]. Saravanakumar M, et al. Oral administration of veratric acid, a constituent of vegetables and fruits, prevents cardiovascular remodelling in hypertensive rats: a functional evaluation. Br J Nutr. 2015 Nov 14;114(9):1385-94. [3]. Shin SW, et al. Antagonist effects of veratric acid against UVB-induced cell damages. Molecules. 2013 May 10;18(5):5405-19.
| Cas No. | 1993-7-2 | SDF | |
| 别名 | 藜芦酸 | ||
| Canonical SMILES | O=C(O)C1=CC=C(OC)C(OC)=C1 | ||
| 分子式 | C9H10O4 | 分子量 | 182.17 |
| 溶解度 | DMSO: 110 mg/mL (603.83 mM); Water: < 0.1 mg/mL (insoluble) | 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 | 5.4894 mL | 27.4469 mL | 54.8938 mL |
| 5 mM | 1.0979 mL | 5.4894 mL | 10.9788 mL |
| 10 mM | 0.5489 mL | 2.7447 mL | 5.4894 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。
Veratric acid Inhibits LPS-Induced IL-6 and IL-8 Production in Human Gingival Fibroblasts
Inflammation 2016 Feb;39(1):237-242.PMID:26329367DOI:10.1007/s10753-015-0243-9.
Veratric acid, one of the major benzoic acid isolated from vegetables and fruits, has been reported to have anti-inflammatory activity. The purpose of this study was to investigate the anti-inflammatory effects of Veratric acid on lipopolysaccharide (LPS)-induced inflammatory response in human gingival fibroblasts (HGFs). HGFs were pretreated with Veratric acid 1 h before LPS stimulation. The productions of IL-6 and IL-8 were detected by ELISA. The expression of iNOS, COX-2, PI3K, AKT, and NF-κB were detected by western blotting. The results showed that Veratric acid inhibited LPS-induced IL-6 and IL-8 production, as well as iNOS and COX-2 expression. Veratric acid also inhibited LPS-induced NF-κB activation. In addition, Veratric acid was found to suppress LPS-induced PI3K and AKT phosphorylation. In conclusion, the anti-inflammatory mechanism of Veratric acid is due to its ability to inhibit PI3K/Akt/NF-κB signaling pathway.
Veratric acid alleviates liver ischemia/reperfusion injury by activating the Nrf2 signaling pathway
Int Immunopharmacol 2021 Dec;101(Pt B):108294.PMID:34749250DOI:10.1016/j.intimp.2021.108294.
Oxidative stress following liver ischemia/reperfusion (I/R) is an important pathological mechanism responsible for liver injury. Veratric acid (VA) is a phenolic benzoic acid that has been reported to have antioxidant properties. However, whether VA has protective effects against liver I/R injury remains unclear. In the present study, a mouse liver I/R injury model was established. VA was administered intragastrically for one week before liver I/R. Biochemical indicators, histological analysis, cell apoptosis, oxidative stress, and pathway proteins were tested to evaluate the protective effects of VA on liver I/R injury. Furthermore, a mouse AML12 hepatocyte hypoxia/reoxygenation (H/R) model was used to explore the underlying mechanism. VA alleviated liver I/R injury, as manifested by decreased alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, liver necrotic area, oxidative stress, and hepatocyte apoptosis. VA pretreatment increased the expression of Nrf2 and its downstream antioxidant proteins heme oxygenase-1 (HO-1) and NADPH quinone oxidoreductase 1 (NQO-1). In addition, VA pretreatment increased AML12 cell activity and decreased oxidative stress; it also decreased the apoptosis induced by H/R. Moreover, the protective effect of VA on hepatocytes was related to the activation of the Nrf2 signaling pathway, and to increases in the Nrf2, HO-1, and NQO-1 protein expression. The inhibition of Nrf2 with ML385 offseted VA-mediated protection in AML12 cells. In conclusion, these results suggest that VA protects the liver from oxidative stress and apoptosis induced by liver I/R injury by activating the Nrf2 signaling pathway.
Veratric acid, a phenolic acid attenuates blood pressure and oxidative stress in L-NAME induced hypertensive rats
Eur J Pharmacol 2011 Dec 5;671(1-3):87-94.PMID:21937012DOI:10.1016/j.ejphar.2011.08.052.
The present study was undertaken to assess the antihypertensive and antioxidant effects of Veratric acid on N(ω)-nitro-L arginine methyl ester (L-NAME) induced hypertensive rats. Hypertension was induced in adult male albino rats of the Wistar strain, weighing 180-220 g, by oral administration of the L-NAME (40 mg/kg body weight/day) in drinking water for 4 weeks. Rats were treated with various doses of Veratric acid (20, 40, 80 mg/kg/day) for four weeks. Hypertension was manifested by considerably increased systolic and diastolic blood pressure and the toxic effect of L-NAME was determined using lipid peroxidative markers (thiobarbituric acid reactive substances and lipid hydroperoxides). We also assessed the activities of enzymatic antioxidants (superoxide dismutase, catalase, and glutathione peroxidase) and measured the levels of non-enzymatic antioxidants (vitamin-C, vitamin-E and reduced glutathione) levels in erythrocytes, plasma and tissues and plasma nitric oxide metabolites (nitrite/nitrate). Oral administration of Veratric acid at the dosage of 40 mg/kg considerably decreased systolic and diastolic blood pressure, lipid peroxidation products; increased plasma nitric oxide levels and showed no toxicity which was measured using hepatic and renal function markers when compared to other doses of Veratric acid (20, 80 mg/kg). In addition, histopathological findings of Veratric acid treated hypertensive rat heart confirmed the biochemical findings of this study. These results suggest that Veratric acid decreased the blood pressure, significantly restored nitric oxide, enzymatic and non-enzymatic antioxidants and reduced lipid peroxidation products and thus exhibits antihypertensive and antioxidant effects against l-NAME induced hypertension.
Veratric acid inhibits iNOS expression through the regulation of PI3K activation and histone acetylation in LPS-stimulated RAW264.7 cells
Int J Mol Med 2015 Jan;35(1):202-10.PMID:25352364DOI:10.3892/ijmm.2014.1982.
In the present study, we investigated regulatory effects of Veratric acid on the production of nitric oxide (NO) in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. NO production was significantly decreased by Veratric acid in the LPS-stimulated RAW264.7 cells in a dose-dependent manner. The reduction in nitric oxide production was induced by the downregulation of inducible NO synthase (iNOS) expression. Veratric acid suppressed the LPS-induced effects on the regulatory and catalytic subunits of phosphoinositide 3-kinase (PI3K), comprised of p85, p110α, p110β and Akt. The acetylation of p300 and the phosphorylation of activating transcription factor 2 (ATF-2) induced by LPS were downregulated following treatment with Veratric acid; similar effects were observed following treatment with LY294002, a specific inhibitor of PI3K/Akt. The LPS-induced expression of histone deacetylase (HDAC)3 decreased to basal levels following treatment with Veratric acid, and its expression was also downregulated by LY294002. In the measurement of histone acetylation levels, the LPS-stimulated acetylation of histone H4 was significantly attenuated by Veratric acid, and was also reduced following the inhibition of PI3K/Akt with LY294002. From our data, it can be concluded that Veratric acid exerts a regulatory effect on LPS-induced iNOS expression. Our results suggest that Veratric acid impedes the PI3K/Akt-mediated histone acetyl-transferase (HAT) activation and HDAC expression induced by LPS, thereby abrogating iNOS expression.
Veratric acid derivatives containing benzylidene-hydrazine moieties as promising tyrosinase inhibitors and free radical scavengers
Bioorg Med Chem 2019 Jun 15;27(12):2644-2651.PMID:31000406DOI:10.1016/j.bmc.2019.04.016.
Tyrosinase enzyme plays a crucial role in melanin biosynthesis and enzymatic browning process of vegetables and fruits. A series of Veratric acid derivatives containing benzylidene-hydrazine moieties with different substitutions were synthesized and their inhibitory effect on mushroom tyrosinase and free radical scavenging activity were evaluated. The results indicated that N'-(4-chlorobenzylidene)-3,4-dimethoxybenzohydrazide (D5) and N'-(2,3-dihydroxybenzylidene)-3,4-dimethoxybenzohydrazide (D12) showed the highest tyrosinase inhibitory activity with IC50 values of 19.72 ± 1.84 and 20.63 ± 0.79 μM, respectively, that were comparable with the IC50 value of kojic acid (19.08 ± 1.21 μM). D12 was also a potent radical scavenger with EC50 value of 0.0097 ± 0.0011 mM. The free radical scavenging activity of D12 was comparable with the standard quercetin. The inhibition kinetic analyzed by Lineweaver-Burk plots revealed that compound D5 was a competitive tyrosinase inhibitor. Molecular docking study was carried out for the derivatives demonstrating tyrosinase inhibitory activity. D5 and D12 possessed the most negative estimated free energies of binding in mushroom tyrosinase active site. Therefore, D5 and D12 could be introduced as potent tyrosinase inhibitors that might be promising leads in medicine, cosmetics and food industry.