Purpurogallin
(Synonyms: 红倍酚) 目录号 : GC38116
A phenol
Cas No.:569-77-7
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
Purpurogallin is a phenol that has been found in D. divisa and a derivative of pyrogallol that has diverse biological activities, including antimicrobial, antioxidant, and enzyme inhibitory properties.1,2,3,4,5,6 It is active against the Gram-positive bacteria S. aureus, methicillin-resistant S. aureus (MRSA), S. epidermidis, and B. subtilis (MICs = 11-110 ?g/ml), the Gram-negative bacteria S. marcescens, P. vulgaris, K. pneumoniae, E. coli, S. typhi, and E. cloacae (MIC = 110 ?g/ml for all), as well as P. falciparum strain FCB1 clone NC-1 (IC50 = 55 ?M).1,3 Purpurogallin (2, 5, and 10 ?M) scavenges 2,2-diphenyl-1-picrylhydrazyl radicals in a cell-free assay and reduces hydrogen peroxide- and radiation-induced production of reactive oxygen species (ROS) in HaCaT keratinocytes.2 It inhibits the activity of EGFR, glutathione-S-transferase (GST), prolyl endopeptidase, and glyoxalase I (IC50s = 27.5, 8, 16, and 50 ?M, respectively), as well as catechol O-methyltransferase (COMT; Ki = 0.074 ?M), in cell-free assays.1,3,4,5,6
1.Inamori, Y., Muro, C., Sajima, E., et al.Biological activity of purpurogallinBiosci. Biotechnol. Biochem.61(5)890-892(1997) 2.Zhen, A.X., Piao, M.J., Hyun, Y.J., et al.Purpurogallin protects keratinocytes from damage and apoptosis induced by ultraviolet B radiation and particulate matter 2.5Biomol. Ther. (Seoul)27(4)395-403(2019) 3.Barnard, J.F., Vander Jagt, D.L., and Honek, J.F.Small molecule probes of glyoxalase I and glyoxalase IIBiochim. Biophys. Acta1208(1)127-135(1994) 4.Abou-Karam, M., and Shier, W.T.Inhibition of oncogene product enzyme activity as an approach to cancer chemoprevention. Tyrosine-specific protein kinase inhibition by purpurogallin from Quercus sp. nutgallPhytother. Res.13(4)337-340(1999) 5.Das, M., Bickers, D.R., and Mukhtar, H.Plant phenols as in vitro inhibitors of glutathione S-transferase(s)Biochem. Biophys. Res. Commun.120(2)427-433(1984) 6.Veser, J.Kinetics and inhibition studies of catechol O-methyltransferase from the yeast Candida tropicalisJ. Bacteriol.169(8)3696-3700(1987)
| Cas No. | 569-77-7 | SDF | |
| 别名 | 红倍酚 | ||
| Canonical SMILES | O=C1C(O)=CC=CC2=CC(O)=C(O)C(O)=C21 | ||
| 分子式 | C11H8O5 | 分子量 | 220.18 |
| 溶解度 | DMSO: 125 mg/mL (567.72 mM) | 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 | 4.5417 mL | 22.7087 mL | 45.4174 mL |
| 5 mM | 0.9083 mL | 4.5417 mL | 9.0835 mL |
| 10 mM | 0.4542 mL | 2.2709 mL | 4.5417 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。
Purpurogallin Protects Keratinocytes from Damage and Apoptosis Induced by Ultraviolet B Radiation and Particulate Matter 2.5
Biomol Ther (Seoul) 2019 Jul 1;27(4):395-403.PMID:30419635DOI:10.4062/biomolther.2018.151.
Purpurogallin, a natural phenol obtained from oak nutgalls, has been shown to possess antioxidant, anticancer, and anti-inflammatory effects. Recently, in addition to ultraviolet B (UVB) radiation that induces cell apoptosis via oxidative stress, particulate matter 2.5 (PM2.5) was shown to trigger excessive production of reactive oxygen species. In this study, we observed that UVB radiation and PM2.5 severely damaged human HaCaT keratinocytes, disrupting cellular DNA, lipids, and proteins and causing mitochondrial depolarization. Purpurogallin protected HaCaT cells from apoptosis induced by UVB radiation and/or PM2.5. Furthermore, Purpurogallin effectively modulates the pro-apoptotic and anti-apoptotic proteins under UVB irradiation via caspase signaling pathways. Additionally, Purpurogallin reduced apoptosis via MAPK signaling pathways, as demonstrated using MAPK-p38, ERK, and JNK inhibitors. These results indicate that Purpurogallin possesses antioxidant effects and protects cells from damage and apoptosis induced by UVB radiation and PM2.5.
Purpurogallin is a novel mitogen-activated protein kinase kinase 1/2 inhibitor that suppresses esophageal squamous cell carcinoma growth in vitro and in vivo
Mol Carcinog 2019 Jul;58(7):1248-1259.PMID:31100197DOI:10.1002/mc.23007.
Purpurogallin is a natural compound that is extracted from nutgalls and oak bark and it possesses antioxidant, anticancer, and anti-inflammatory properties. However, the anticancer capacity of Purpurogallin and its molecular target have not been investigated in esophageal squamous cell carcinoma (ESCC). Herein, we report that Purpurogallin suppresses ESCC cell growth by directly targeting the mitogen-activated protein kinase kinase 1/2 (MEK1/2) signaling pathway. We found that Purpurogallin inhibits anchorage-dependent and -independent ESCC growth. The results of in vitro kinase assays and cell-based assays indicated that Purpurogallin also strongly attenuates the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway and also directly binds to and inhibits MEK1 and MEK2 activity. Furthermore, Purpurogallin contributed to S and G2 phase cell cycle arrest by reducing cyclin A2 and cyclin B1 expression and also induced apoptosis by activating poly (ADP ribose) polymerase (PARP). Notably, Purpurogallin suppressed patient-derived ESCC tumor growth in an in vivo mouse model. These findings indicated that Purpurogallin is a novel MEK1/2 inhibitor that could be useful for treating ESCC.
Purpurogallin--a natural and effective hepatoprotector in vitro and in vivo
Biochem Cell Biol 1991 Oct-Nov;69(10-11):747-50.PMID:1799443DOI:10.1139/o91-113.
Purpurogallin is a plant phenol that is sometimes added as an oxidation retardant to fats-oils or to certain fuels or lubricants. However, it was unknown if Purpurogallin is cytoprotective. Here we examined this issue, both in isolated hepatocytes and in vivo. From 0.5 to 2.0 mM, Purpurogallin prolongs survival of rat hepatocytes substantially against oxyradicals generated with xanthine oxidase and hypoxanthine. The protection was dose dependent and surpassed that given by such antioxidants as ascorbate, mannitol, superoxide dismutase, catalase, and Trolox, when each was examined at or near its optimal concentration in the same system. When 1.5, 3, and 6 mumol of Purpurogallin in saline were infused into rats with postischemic livers shortly before reperfusion, the mean hepatic salvages were 42, 76, and 86%, respectively. Such salvage effects would rank Purpurogallin highly among the hepatoprotectors known. Over the range of 31 to 500 microM, Purpurogallin inhibited the rate of O2 consumption in the xanthine oxidase reaction by approximately 90%, which was 2- to several-fold higher than the inhibition elicited by allopurinol over the same concentrations. Thus, Purpurogallin is an effective natural hepatoprotector that may operate partly or principally as an inhibitor of xanthine oxidase.
Purpurogallin improves neurological functions of cerebral ischemia and reperfusion mice by inhibiting endoplasmic reticulum stress and neuroinflammation
Int Immunopharmacol 2022 Oct;111:109057.PMID:35964408DOI:10.1016/j.intimp.2022.109057.
Background: Purpurogallin (PPG) has been testified to have neuroprotective effects. This study intends to probe the neuroprotection of PPG on cerebral ischemia/reperfusion (I/R) injury and its potential mechanism. Methods: C57/B6 mice, BV2 microglia and HT22 hippocampal neurons were used for in-vivo and in-vitro experiments. I/R injury models were constructed using middle cerebral artery occlusion (MCAO/R) and oxygen-glucose deprivation/reoxygenation (OGD/R), respectively. The expression of apoptosis and inflammatory proteins, and endoplasmic reticulum (ER) stress proteins were gauged by Western blotting (WB). The contents of inflammatory cytokines in OGD/R-induced BV2 microglia were testified by enzyme-linked immunosorbent assay (ELISA). Cell counting kit-8 (CCK-8), TUNEL assay and flow cytometry (FCM) were utilized to examine the viability and apoptosis of cells. The neurological, learning and memory functions were evaluated by the modified neurological severity score (mNSS) and water maze experiment. 2, 3, 5-triphenyltetrazole chloride (TTC) staining was utilized to calculate the volume of cerebral infarction and cerebral edema in the peri-infarct area. Apoptosis-related proteins, inflammation-related proteins and ER stress proteins were gauged by WB. ELISA was conducted to verify inflammatory cytokines. Results: PPG treatment notably abated the expression of ER stress proteins and inflammatory factors in OGD/R-induced BV2 microglia and boosted HT22 neuron's viability and eased their apoptosis in comparison to the control group. In vivo, PPG treatment signally lessened cerebral infarct area, cerebral edema, and neurological deficit scores in MCAO/R mice. Additionally, PPG caused a dramatic decline in neuronal apoptosis and levels of ER stress proteins and inflammatory factors in the brain's peri-infarct region of MCAO/R mice. Mechanically, PPG blocked the TLR4/NF-κB pathway in OGD/R-induced BV2, HT22 neurons, and the MCAO/R mice. Conclusion: PPG attenuates brain I/R damage probably by suppressing ER stress and neuroinflammation via inactivation of the TLR4/NF-κB pathway, suggesting that PPG may be a candidate drug for treating cerebral I/R injury.
Inhibitory Effect of Purpurogallin on Osteoclast Differentiation in Vitro through the Downregulation of c-Fos and NFATc1
Int J Mol Sci 2018 Feb 17;19(2):601.PMID:29463002DOI:10.3390/ijms19020601.
Purpurogallin, a benzotropolone-containing natural compound, has been reported to exhibit numerous biological and pharmacological functions, such as antioxidant, anticancer, and anti-inflammatory effects. In this study, we enzymatically synthesized Purpurogallin from pyrogallol and investigated its role in receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis. Purpurogallin attenuated the formation of multinucleated tartrate-resistant acid phosphatase (TRAP)-positive osteoclasts from bone marrow macrophages (BMMs) without causing cytotoxicity, and suppressed upregulation of osteoclast-specific markers, including TRAP (Acp5), cathepsin K (Ctsk), and dendritic cell-specific transmembrane protein (Dcstamp). However, Purpurogallin did not affect the bone resorbing function of mature osteoclasts evident by the resorption pit assay. Activation of mitogen-activated protein kinases, Akt and IkB pathways in RANK signaling were not altered by Purpurogallin, whereas the expression of c-Fos and NFATc1, key transcriptional regulators in osteoclastogenesis, was dramatically inhibited by Purpurogallin. Purpurogallin also significantly reduced the expression level of B lymphocyte-induced maturation protein-1 (Blimp1) gene (Prdm1). Further, downregulation of Blimp1 led to forced expression of anti-osteoclastogenic genes, including interferon regulatory factor-8 (Irf8) and B-cell lymphoma 6 (Bcl6) genes. Taken together, our data suggested that Purpurogallin inhibits osteoclast differentiation via downregulation of c-Fos and NFATc1.