Purpurin
(Synonyms: 羟基茜草素) 目录号 : GC44777A naturally occurring pigment with anti-mutagenic effects
Cas No.:81-54-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Purpurin is a naturally occurring reddish-yellow pigment found in madder root (R. tinctorum) that has been used both in herbal remedies and as food coloring. It can also be synthetically derived from 9,10-anthraquinone. Purpurin is protective against a number of food-derived heterocyclic amines in bacterial mutagenicity assays through its inhibition of CYP450-dependent N-hydroxylation and reduction of N-hydroxylamines. Purpurine can also inhibit (IC50 = 6.6 μM) spermidine-induced autoactivation of plasma hyaluronan-binding protein, a serine protease that can activate coagulation factor VII and prourokinase.
| Cas No. | 81-54-9 | SDF | |
| 别名 | 羟基茜草素 | ||
| Canonical SMILES | O=C1C2=C(O)C=C(O)C(O)=C2C(C3=C1C=CC=C3)=O | ||
| 分子式 | C14H8O5 | 分子量 | 256.2 |
| 溶解度 | DMF: 0.5 mg/ml,DMSO: 0.5 mg/ml | 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 | 3.9032 mL | 19.516 mL | 39.032 mL |
| 5 mM | 0.7806 mL | 3.9032 mL | 7.8064 mL |
| 10 mM | 0.3903 mL | 1.9516 mL | 3.9032 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。
Purpurin suppresses atopic dermatitis via TNF-α/IFN-γ-induced inflammation in HaCaT cells
Int J Immunopathol Pharmacol 2022 Jan-Dec;36:3946320221111135.PMID:35794850DOI:10.1177/03946320221111135.
Objective: We investigated whether Purpurin inhibits various pathways of inflammation leading to atopic dermatitis. Introduction: 1,2,4-Trihydroxyanthraquinone, commonly called Purpurin, is an anthraquinone that is a naturally occurring red/yellow dye. Purpurin is a highly antioxidative anthraquinone and previous studies have reported antibacterial, anti-tumor, and anti-oxidation activities in cells and animals. However, the skin inflammatory inhibition activity mechanism study of Purpurin has not been elucidated in vitro. Methods: In this study, we investigated the anti-inflammatory activity of Purpurin in HaCaT (human keratinocyte) cell lines stimulated with a mixture of tumor necrosis factor-alpha (TNF-α)/Interferon-gamma (IFN-γ). The inhibitory effect of Purpurin on cytokines (IL-6, IL-8, and IL-1β) and chemokine (TARC, MDC, and RANTES) was confirmed by ELISA and RT-qPCR. We investigated each signaling pathway and the action of inhibitors through western blots. Results: The expression levels of cytokines and chemokines were dose-dependently suppressed by Purpurin treatment in TNF-α/IFN-γ-induced HaCaT cells from ELISA and real-time PCR. Purpurin also inhibited protein kinase B (AKT), mitogen-activated protein kinase (MAPKs), and nuclear factor kappa-light-chain-enhancer of activated B (NF-κB) activation in TNF-α/IFN-γ-stimulated HaCaT cells. Additionally, there was a synergistic effect when Purpurin and inhibitor were applied together, and inflammation was dramatically reduced. Conclusion: Therefore, these results demonstrate that Purpurin exhibits anti-inflammatory and anti-atopic dermatitis activity in HaCaT cells.
Purpurin: A natural anthraquinone with multifaceted pharmacological activities
Phytother Res 2020 Nov 30.PMID:33254282DOI:10.1002/ptr.6965.
Purpurin is a naturally occurring anthraquinone isolated from the roots of Rubia cordifolia. Historically, it has been used as a red dye. However, its photosensitizing property and biological effects have deciphered its novel application. Purpurin shows antigenotoxic, anticancer, neuromodulatory, and antimicrobial potential associated with antioxidant action in in vivo and in vitro experiments. A robust antioxidant nature of Purpurin is responsible for the majority of its pharmacological effects. It produces anti-inflammatory activity by reducing oxidative stress, which is a fundamental property to target diseases involving endoplasmic reticulum and mitochondrial stress. It can cross the blood-brain barrier and produce neuroprotective effects, including antidepressant and anti-Alzheimer action. It shows antimutagenic property via inhibiting essential CYP-450 enzymes. Interestingly, it gets photosensitized by UV-light and produces target-specific ROS-dependent apoptosis in cancer cells. Therefore, it owns cell killing and cell survival potential subject to the influence of external conditions. Hitherto, limited research studies are performed with Purpurin to understand its therapeutic potential. Hence, this review describes and discusses different in vivo, in vitro, and in silico studies performed using Purpurin. It also covers physicochemical, pharmacokinetics, and toxicology aspects of Purpurin. Moreover, in the end, the prospect of Purpurin in the management of cancer has also been proposed.
Purpurin ameliorates alcohol-induced hepatotoxicity by reducing ROS generation and promoting Nrf2 expression
Life Sci 2022 Nov 15;309:120964.PMID:36115584DOI:10.1016/j.lfs.2022.120964.
Introduction and aim: Purpurin, a naturally occurring anthraquinone isolated from the roots of Rubia cordifolia, exhibits anti-cancer, anti-genotoxic, anti-microbial, neuromodulatory and photodynamic activity. However, Purpurin's in vivo and in vitro antioxidant mechanism remains unexplored. The present study explores the anti-oxidative mechanism of Purpurin under the influence of alcohol using in vivo and in vitro test systems. Methods: Mice hepatocytes and alcohol-induced liver toxicity model were used to evaluate the effect of Purpurin. The non-enzymatic and enzymatic oxidative stress markers were estimated by the colorimetric method. The reactive oxygen species (ROS) were quantified in mitochondria and cells using flow cytometer. Real-time PCR and western blotting were used to quantify cytochrome 450 subtype 2E1 (CYP2E1) and Nrf2 expression in the liver tissue of mice. In silico studies were performed through receptor-ligand binding interaction. Key findings: Purpurin effectively reduced total cellular and mitochondrial ROS in primary hepatocytes and WRL-68 cells. It prevented alcohol-induced ROS-dependent biochemical and cellular insults observed by analysing the serum glutamic pyruvic transaminase (SGPT), glutamic-oxaloacetic transaminase (SGOT) levels and CYP2E1 expression in liver tissue of alcohol-administered mice. Moreover, it also restored the activity of antioxidant enzymes. Its antioxidant effect was established by glutathione and ROS-dependent mechanisms using buthionine sulfoximine and N-acetyl cysteine. Along with alcohol, Purpurin up-regulated Nrf2 expression in hepatocytes. Significance: This work confirmed the ameliorative effect of Purpurin for alcohol-induced hepatotoxicity by drabbing free radicals and curbing oxidative stress via activation of antioxidant signalling pathways.
Copper-mediated DNA damage caused by Purpurin, a natural anthraquinone
Genes Environ 2022 May 9;44(1):15.PMID:35527257DOI:10.1186/s41021-022-00245-2.
Background: Purpurin (1,2,4-trihydroxy-9,10-anthraquinone), a natural red anthraquinone pigment, has historically been used as a textile dye. However, Purpurin induced urinary bladder tumors in rats, and displayed a mutagenic activity in assay using bacteria and mammalian cells. Many carcinogenic dyes are known to induce bladder cancers via DNA adduct formation, but carcinogenic mechanisms of Purpurin remain unknown. In this study, to clarify the mechanism underlying carcinogenicity of Purpurin, copper-mediated DNA damage induced by Purpurin was examined using 32P-labeled DNA fragments of human genes relevant to cancer. Furthermore, we also measured 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG), an indicator of oxidative DNA damage, in calf thymus DNA. Results: Purpurin plus Cu(II) cleaved 32P-labeled DNA fragments only under piperidine treatment, indicating that Purpurin caused base modification, but not breakage of the DNA backbone. In the absence of Cu(II), Purpurin did not induce DNA cleavage even with piperidine treatment. Purpurin plus Cu(II) caused piperidine-labile sites predominantly at G and some T residues. Bathocuproine, a Cu(I) chelator, completely prevented the occurrence of piperidine-labile sites, indicating a critical role of Cu(I) in piperidine-labile sites induced by Purpurin plus Cu(II). On the other hand, methional, a scavenger of a variety of reactive oxygen species (ROS) and catalase showed limited inhibitory effects on the induction of piperidine-labile sites, suggesting that ROS could not be major mediators of the purpurin-induced DNA damage. Considering reported DNA adduct formation by quinone metabolites of several carcinogenic agents, quinone form of Purpurin, which is possibly generated via Purpurin autoxidation accompanied by Cu(I)/Cu(II) redox cycle, might lead to DNA adducts and piperidine-labile sites. In addition, we measured contents of 8-oxodG. Purpurin moderately but significantly increased 8-oxodG in calf thymus DNA in the presence of Cu(II). The 8-oxodG formation was inhibited by catalase, methional and bathocuproine, suggesting that Cu(I)-hydroperoxide, which was generated via Cu(I) and H2O2, caused oxidative DNA base damage. Conclusions: We demonstrated that Purpurin induces DNA base damage possibly mediated by Cu(I)/Cu(II) redox cycle both with and without ROS generation, which are likely to play an important role in its carcinogenicity.
Microenvironment-Responsive Prodrug-Induced Pyroptosis Boosts Cancer Immunotherapy
Adv Sci (Weinh) 2021 Dec;8(24):e2101840.PMID:34705343DOI:10.1002/advs.202101840.
The absence of tumor antigens leads to a low response rate, which represents a major challenge in immune checkpoint blockade (ICB) therapy. Pyroptosis, which releases tumor antigens and damage-associated molecular patterns (DAMPs) that induce antitumor immunity and boost ICB efficiency, potentially leads to injury when occurring in normal tissues. Therefore, a strategy and highly efficient agent to induce tumor-specific pyroptosis but reduce pyroptosis in normal tissues is urgently required. Here, a smart tumor microenvironmental reactive oxygen species (ROS)/glutathione (GSH) dual-responsive nano-prodrug (denoted as MCPP) with high paclitaxel (PTX) and photosensitizer Purpurin 18 (P18) loading is rationally designed. The ROS/GSH dual-responsive system facilitates the nano-prodrug response to high ROS/GSH in the tumor microenvironment and achieves optimal drug release in tumors. ROS generated by P18 after laser irradiation achieves controlled release and induces tumor cell pyroptosis with PTX by chemo-photodynamic therapy. Pyroptotic tumor cells release DAMPs, thus initiating adaptive immunity, boosting ICB efficiency, achieving tumor regression, generating immunological memory, and preventing tumor recurrence. Mechanistically, chemo-photodynamic therapy and control-release PTX synergistically induce gasdermin E (GSDME)-related pyroptosis. It is speculated that inspired chemo-photodynamic therapy using the presented nano-prodrug strategy can be a smart strategy to trigger pyroptosis and augment ICB efficiency.