|Source:||The herbs of Onychium japonicum|
|Biological Activity or Inhibitors:||1. 3,4-Dihydroxybenzoic acid exhibits scavenging actions against the 1,1-diphenyl-2-picrylhydrazyl radical, the superoxide anion, and the hydroxyl radical.
2. 3,4-Dihydroxybenzoic acid isolates from a green alga protects human keratinocytes against UVB-induced oxidative stress and apoptosis.
3. 3,4-Dihydroxybenzoic acid has been shown to prevent carcinogenesis or antitumor growth in vivo, it has apoptotic effect on human gastric carcinoma cells involving JNK/p38 MAPK signaling activation.
4. 3,4-Dihydroxybenzoic acid can prevent Abeta (25-35)-induced neuronal cell damage by interfering with the increase of [Ca(2+)](c), and then by inhibiting glutamate release, generation of ROS and caspase-3 activity.
5. 3,4-Dihydroxybenzoic acid has protection against Adriamycin cytotoxicity and inhibition of DNA topoisomerase II activity.
6. 3,4-Dihydroxybenzoic acid has nematicidal activity against Meloidogyne incognita.
7. 3,4-Dihydroxybenzoic acid shows significant antioxidant using DPPH and antimicrobial activities.
|Solvent:||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: firstname.lastname@example.org
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||6.4893 mL||32.4465 mL||64.8929 mL||129.7859 mL||162.2323 mL|
|5 mM||1.2979 mL||6.4893 mL||12.9786 mL||25.9572 mL||32.4465 mL|
|10 mM||0.6489 mL||3.2446 mL||6.4893 mL||12.9786 mL||16.2232 mL|
|50 mM||0.1298 mL||0.6489 mL||1.2979 mL||2.5957 mL||3.2446 mL|
|100 mM||0.0649 mL||0.3245 mL||0.6489 mL||1.2979 mL||1.6223 mL|
Appl Biochem Biotechnol. 2014 Mar;172(5):2582-92.
|Protective effect of 3,4-dihydroxybenzoic acid isolated from Cladophora wrightiana Harvey against ultraviolet B radiation-induced cell damage in human HaCaT keratinocytes.[Pubmed: 24414942]|
|The aim of the present study was to elucidate the protective properties of 3,4-Dihydroxybenzoic acid (DBA) isolated from Cladophora wrightiana Harvey (a green alga) against ultraviolet B (UVB)-induced damage to human HaCaT keratinocytes. 3,4-Dihydroxybenzoic acid exhibited scavenging actions against the 1,1-diphenyl-2-picrylhydrazyl radical, the superoxide anion, and the hydroxyl radical. Furthermore, 3,4-Dihydroxybenzoic acid decreased the levels of intracellular reactive oxygen species generated by hydrogen peroxide or UVB treatment of the cells. 3,4-Dihydroxybenzoic acid also decreased the UVB-augmented levels of phospho-histone H2A.X and the extent of comet tail formation, which are both indications of DNA damage. Taken together, these results demonstrate that 3,4-Dihydroxybenzoic acid isolated from a green alga protects human keratinocytes against UVB-induced oxidative stress and apoptosis.|
Microb Pathog. 2013 Jun-Jul;59-60:52-9.
|Nematicidal activity of 3,4-dihydroxybenzoic acid purified from Terminalia nigrovenulosa bark against Meloidogyne incognita.[Pubmed: 23603737]|
|In this study, the 3,4-Dihydroxybenzoic acid (3,4-DHBA) from Terminalia nigrovenulosa bark (TNB) was purified and its in vitro nematicidal activity was investigated against Meloidogyne incognita. The purification of 3,4-Dihydroxybenzoic acid used a silica gel column and Sephadex LH-20 chromatography combined with thin-layer chromatography and high performance liquid chromatography. Structural identification of the 3,4-Dihydroxybenzoic acid was conducted using (1)H nuclear magnetic resonance (NMR), (13)C NMR, and liquid chromatography time-of-flight mass spectrometry. Nematicidal activity bioassays revealed that 3,4-Dihydroxybenzoic acid treatment resulted in 33.3, 47.5, 72.5 and 94.2% J2 mortality at 0.125, 0.25, 0.5 and 1.0 mg/ml, respectively after 12 h incubation. J2 mortality was increased significantly (P < 0.0001) with increasing incubation time in the range of 54.2-94.2% from 3 to 9 h after incubation with 3,4-Dihydroxybenzoic acid (1.0 mg/ml), but with no significant difference observed where the incubation time was increased from 9 to 12 h. The 3,4-Dihydroxybenzoic acid treatment resulted in 33.3, 65.0, 76.7 and 85.0% hatch inhibition at 0.125, 0.25, 0.5 and 1.0 mg/ml, respectively, 3 days after incubation. Changes in the shape of the eggs were determined after incubation for 1 day with a 3,4-Dihydroxybenzoic acid concentration of 1.0 mg/ml.|
Indonesian Journal of Chemistry, 2012, 12(3):273-8.
|3,4-dihydroxybenzoic acid and 3,4-dihydroxybenzaldehyde from the fern Trichomanes chinense L.; isolation, antimicrobial and antioxidant properties.[Reference: WebLink]|
|3,4-Dihydroxybenzoic acid (1) and 3,4-dihydroxybenzaldehyde (2) have been isolated from ethyl acetate fraction of methanolic fractions of leaves, stems and roots of the fern Trichomanes chinense L. (Hymenophyllaceae). These two compounds also showed significant antioxidant using DPPH and antimicrobial activities using the disc diffusion assay.|
Neurosci Lett. 2007 Jun 13;420(2):184-8.
|3,4-dihydroxybenzoic acid from Smilacis chinae rhizome protects amyloid beta protein (25-35)-induced neurotoxicity in cultured rat cortical neurons.[Pubmed: 17531386 ]|
|The neuroprotective effect of 3,4-Dihydroxybenzoic acid (3,4-DHBA) isolated from Smilacis chinae rhizome against Abeta (25-35)-induced neurotoxicity on cultured rat cortical neurons was found in this study. The protective effect of 3,4-DHBA against Abeta (25-35)-induced neuronal cell death was investigated by measuring cell viability via a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining. 3,4-DHBA (1 and 10 microM) concentration-dependently inhibited 10 microM Abeta (25-35)-induced neuronal apoptotic death. 3,4-DHBA (1 and 10 microM) inhibited 10 microM Abeta (25-35)-induced elevation of cytosolic Ca(2+) concentration ([Ca(2+)](c)), which was measured by a fluorescent dye, Fluo-4 AM. 3,4-DHBA also inhibited glutamate release into medium, reactive oxygen species (ROS) generation, and caspase-3 activation, which were induced by 10 microM Abeta (25-35). These results suggest that 3,4-DHBA prevents Abeta (25-35)-induced neuronal cell damage by interfering with the increase of [Ca(2+)](c), and then by inhibiting glutamate release, generation of ROS and caspase-3 activity.|
Int J Cancer. 2007 Jun 1;120(11):2306-16.
|Apoptotic effect of 3,4-dihydroxybenzoic acid on human gastric carcinoma cells involving JNK/p38 MAPK signaling activation.[Pubmed: 17304508 ]|
|3,4-Dihydroxybenzoic acid (protocatechuic acid, PCA) is discussed to represent antioxidative food components in a human diet rich in fruits and vegetables, and has been shown to prevent carcinogenesis or antitumor growth in vivo. However, the molecular mechanisms involved in chemopreventive activity of PCA are poorly understood. In this study, investigations were conducted to examine the detailed signaling pathway involved in PCA-induced apoptosis in human gastric adenocarcinoma (AGS) cells. The data from cell viability assay showed that PCA exhibited the antiproliferation effect on AGS cells in a time- and dose-dependent manner. The occurrence of apoptosis induced by PCA was confirmed by morphological and biochemical features, including apoptotic bodies formation and an increase in the distribution of hypodiploid phase. Molecular data showed the effect of PCA in AGS cells might be mediated via sustained phosphorylation and activation of JNK and p38 mitogen-activating protein kinases (MAPK), but not ERK. Treatment with pharmacological inhibitors or transfection with the mutant p38 or/and JNK expression vector reduced PCA-mediated apoptosis and the JNK/p38 MAPK-related proteins phosphorylation and expression, including ATF-2, c-Jun, FasL, Fas, p53 and Bax. Preincubation with Nok-1 monoclonal antibody, which is inhibitory to Fas signaling, interfered with PCA-induced cleavage of procaspase and sensitization to anti-APO-induced apoptosis. These results suggest the possible involvement of multiple signaling pathways from the MAPK to the subsequent mitochondria- and/or Fas-mediated caspase activation are potential requirements for PCA-induced AGS apoptosis. Further, PCA effectively induced JNK/p38 activation in PCA-response cell lines. Taken together, our data present the first evidence of PCA as an apoptosis inducer in AGS cells, even in tumor cells of digestive organs, and provide a new mechanism for its anticancer activity.|
Int J Oncol. 2003 Jul;23(1):159-63.
|Protection against Adriamycin cytotoxicity and inhibition of DNA topoisomerase II activity by 3,4-dihydroxybenzoic acid.[Pubmed: 12792789]|
|The mechanism of Adriamycin (ADR) induced cytotoxicity is not completely understood. While a variety of mechanisms have been proposed, the production of free radicals by redox cycling of the semiquinone has been implicated in cytotoxicity, specifically for cardiotoxicity. To determine whether a scavenger of free radicals would modify the cytotoxicity of ADR, the benzoic acid derivative 3,4-Dihydroxybenzoic acid (DHB) was investigated for its ability to protect against ADR-induced cytotoxicity and DNA double strand breaks in Chinese hamster V79 cells. V79 cells were treated with ADR, or its non-redox cycling analog iminodaunomycin, in the presence or absence of DHB. DHB provided significant protection (dose-modifying factor greater than 2.5 for ADR, and nearly 2 for iminodaunomycin) and also caused a dose-dependent decrease in DNA double strand breaks as measured by pulsed field gel electrophoresis. Assays of topoisomerase II activity showed that DHB inhibited topoisomerase II in a concentration-dependent manner, but did not inhibit topoisomerase I. Another non-toxic topoisomerase II inhibitor, the radioprotector WR-1065, also protected against ADR-induced cytotoxicity. These data identify DHB as a non-toxic inhibitor of DNA topoisomerase II and suggest that much of the cytotoxicity of ADR in actively growing V79 cells is due to mechanisms other than redox cycling by the semiquinone.|