Urolithin B
(Synonyms: 尿石素B) 目录号 : GC38679
A metabolite of ellagic acid
Cas No.:1139-83-9
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
Urolithin B is a metabolite of the polyphenolic antioxidant ellagic acid that has diverse biological activities.1,2,3,4 It is formed from ellagic acid via several intermediates by gut microbiota.1 Urolithin B reduces the levels of advanced glycation end products (AGEs) in a cell-free assay in a concentration-dependent manner.2 It inhibits aromatase activity in human placental microsomes and aromatase-sensitive MCF-7 (MCF-7aro) human breast cancer cells when used at concentrations of 47 and 4.7 ?M, respectively.3 Urolithin B (1.18-4.7 nM) inhibits testosterone-induced proliferation of MCF-7aro cells. It also inhibits LPS-induced increases in inducible nitric oxide synthase (iNOS), TNF-α, IL-6, IL-1β, and COX-2, as well as increases levels of IL-10, in BV-2 microglia when used at concentrations of 50 and 100 ?M.4
1.Tomás-Barberán, F.A., González-Sarrías, A., García-Villalba, R., et al.Urolithins, the rescue of "old" metabolites to understand a "new" concept: Metabotypes as a nexus among phenolic metabolism, microbiota dysbiosis, and host health statusMol. Nutr. Food Res.61(1)(2017) 2.Liu, W., Ma, H., Frost, L., et al.Pomegranate phenolics inhibit formation of advanced glycation endproducts by scavenging reactive carbonyl speciesFood Funct.5(11)2996-3004(2014) 3.Adams, L.S., Zhang, Y., Seeram, N.P., et al.Pomegranate ellagitannin-derived compounds exhibit antiproliferative and antiaromatase activity in breast cancer cells in vitroCancer Prev. Res. (Phila.)3(1)108-113(2010) 4.Lee, G., Park, J.-S., Lee, E.-J., et al.Anti-inflammatory and antioxidant mechanisms of urolithin B in activated microgliaPhytomedicine5550-57(2019)
| Cas No. | 1139-83-9 | SDF | |
| 别名 | 尿石素B | ||
| Canonical SMILES | O=C1C2=CC=CC=C2C3=CC=C(O)C=C3O1 | ||
| 分子式 | C13H8O3 | 分子量 | 212.2 |
| 溶解度 | DMSO: 250 mg/mL (1178.13 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 | 4.7125 mL | 23.5627 mL | 47.1254 mL |
| 5 mM | 0.9425 mL | 4.7125 mL | 9.4251 mL |
| 10 mM | 0.4713 mL | 2.3563 mL | 4.7125 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。
Urolithin B suppressed osteoclast activation and reduced bone loss of osteoporosis via inhibiting ERK/NF-κB pathway
Cell Prolif 2022 Oct;55(10):e13291.PMID:35708050DOI:10.1111/cpr.13291.
Objectives: The main target of current drugs for alleviating bone loss is osteoclasts. However, the long-term application of such drugs will also cause side effects. Therefore, it is of great need to develop new and safer therapeutics for osteoporosis. In recent years, drug development based on gut microbiota has gradually attracted attention. This manuscript investigates the inhibitory effect of Urolithin B (UB) on osteoclastogenesis and differentiation in vitro and in ovariectomized (OVX) mice. Materials and methods: CCK-8 was used to analyse the cytotoxicity of UB; BMMs cells were differentiated into osteoclasts by RANKL, and respectively treated with 1, 5, and 25 μmol/L UB during this process. After one week of intervention, tartrate-resistant acid phosphatase (TRAP) staining was used to analyse the number and average area of osteoclasts. F-actin staining and immunofluorescence staining were conducted to evaluate the morphology and function of osteoclasts. Bone resorption function of osteoclasts was detected by Pit Formation Assay. The expression of osteoclast-related protein genes in RAW264.7 cells were investigated via western blot and RT-PCR assays. Western blot analysis of RANKL-mediated activation of MAPK/NF-κB pathway after 0, 5, 15, 30, 60 min of intervention. For in vivo experiments, OVX mice received intraperitoneal injection of 10, 50 mg/kg every two days, 8 weeks later, the femurs of mice were taken for morphological analysis, and the serum content of CTX-1, a bone metabolism index, was analysed. Results: UB could inhibit the osteoclast differentiation of rankl-induced bone marrow macrophages (BMMs) and RAW264.7 cells in vitro, suppress the uptake activity of hydroxyapatite and expression of osteoclast-related gene MMP9, CTSK, NFATc1 and c-fos. Furthermore, UB repressed the rankl-induced phosphorylation and degradation of IκB and the phosphorylation of P65 in the NF-κB pathway of RAW264.7 cells, and also down-regulated the phosphorylation level of ERK in the MAPK pathway. For in vivo studies, UB-treated OVX mice showed more significant improved various parameters of distal femur compared with the control group, with fewer NFATc1, MMP9 and TRAP-positive osteoclasts in bone tissues, and less serum content of CTX-1. Conclusion: Urolithin B attenuated bone loss in OVX mice by inhibiting the formation and activation of osteoclasts via down-regulation of the ERK/NF-κB signalling pathway.
Urolithin B, a gut microbiota metabolite, protects against myocardial ischemia/reperfusion injury via p62/Keap1/Nrf2 signaling pathway
Pharmacol Res 2020 Mar;153:104655.PMID:31996327DOI:10.1016/j.phrs.2020.104655.
Ischemia/reperfusion (IR) induces additional damage during the restoration of blood flow to ischemic myocardium. Urolithin B (UB) is one of the gut metabolites of ellagitannins, a class of antioxidant polyphenols, which was found to be protective against oxidative stress in multiple organs. However, the role of UB in cardiovascular disease remains elusive. Adult Sprague Dawley rats were subjected to left anterior descending artery ligation for 30 min followed by 120 min of reperfusion, with or without UB treatment. In vitro, the H9c2 cardiomyocytes were subjected to hypoxia (94 %N2/5 %CO2/1 %O2) for 3 h, followed by reoxygenation (74 %N2/5 %CO2/21 %O2) for 3 h (HR). UB was found to decrease myocardial infarct size and attenuate the cardiac dysfunction in the rats after IR, and protect against HR injury in H9c2 cardiomyocytes. Mechanistically, UB inhibited autophagy by activating Akt/mTOR/ULK1 pathway and protected against oxidative stress and caspase 3-dependent cell apoptosis. In particular, UB induced accumulation of p62 and its interaction with Keap1, which promoted Nrf2 nuclear translocation during HR insult. Of note, the protection of UB against superoxide production and apoptotic cell death was compromised with Nrf2 gene silencing. Taken together, our findings suggested that UB protected against myocardial IR injury at least partially via the p62/Keap1/Nrf2 signaling pathway, which highlights the potential of UB as a novel therapy for ischemic heart disease.
Urolithin B: Two-way attack on IAPP proteotoxicity with implications for diabetes
Front Endocrinol (Lausanne) 2022 Dec 15;13:1008418.PMID:36589826DOI:10.3389/fendo.2022.1008418.
Introduction: Diabetes is one of the major metabolic diseases worldwide. Despite being a complex systemic pathology, the aggregation and deposition of Islet Amyloid Polypeptide (IAPP), or amylin, is a recognized histopathological marker of the disease. Although IAPP proteotoxicity represents an important trigger of β-cell dysfunction and ultimately death, its exploitation as a therapeutic tool remains underdeveloped. The bioactivity of (poly)phenols towards inhibition of pathological protein aggregation is well known, however, most of the identified molecules have limited bioavailability. Methods: Using a strategy combining in silico, cell-free and cell studies, we scrutinized a unique in-house collection of (poly)phenol metabolites predicted to appear in the human circulation after (poly)phenols ingestion. Results: We identified Urolithin B as a potent inhibitor of IAPP aggregation and a powerful modulator of cell homeostasis pathways. Urolithin B was shown to affect IAPP aggregation pattern, delaying the formation of amyloid fibrils and altering their size and morphology. The molecular mechanisms underlying urolithin B-mediated protection include protein clearance pathways, mitochondrial function, and cell cycle ultimately rescuing IAPP-mediated cell dysfunction and death. Discussion: In brief, our study uncovered Urolithin B as a novel small molecule targeting IAPP pathological aggregation with potential to be exploited as a therapeutic tool for mitigating cellular dysfunction in diabetes. Resulting from the colonic metabolism of dietary ellagic acid in the human body, Urolithin B bioactivity has the potential to be explored in nutritional, nutraceutical, and pharmacological perspectives.
Recent Advances and Perspectives on the Health Benefits of Urolithin B, A Bioactive Natural Product Derived From Ellagitannins
Front Pharmacol 2022 Jun 22;13:917266.PMID:35814202DOI:10.3389/fphar.2022.917266.
Urolithin (Uro) B is a natural compound produced by gut bacteria from ingested ellagitannins (ETs) and ellagic acid (EA), complex polyphenols abundant in foods such as pomegranates, raspberries, blueberries and chestnuts. Uro B has recently garnered considerable attention owing to its wide range of nutraceutical effects and relatively high potency. According to several studies, Uro B prevents the development of hyperlipidemia, cardiovascular disease (CVD) and tumors due to its strong antioxidant and anti-inflammatory properties. Many reviews have systematically summarized the health benefits and pharmacological activities of ETs, EA and urolithins (especially Uro A) while available reviews or detailed summaries on the positive impact of Uro B are rarer. Here, we sought to review the pharmacological activity, mechanism of action, regulation of immune function and its associated diseases and preventive potential of Uro B to elucidate its function as a nutritional agent in humans.
Urolithin B, a Gut Microbiota Metabolite, Reduced Susceptibility to Myocardial Arrhythmic Predisposition after Hypoxia
Dis Markers 2022 Feb 8;2022:6517266.PMID:35178131DOI:10.1155/2022/6517266.
Cardiomyocyte apoptosis, neural remodeling, and gap junction channel change play critical roles in ventricular arrhythmia (VA) after acute myocardial infarction (AMI). Urolithin B (UB), one of the gut metabolites of ellagitannins, a class of antioxidant polyphenols, has various biological activities, but its direct role in cardiomyocyte apoptosis, neural remodeling, and gap junction channel change after AMI remains elusive. We investigated whether Urolithin B reduced susceptibility of myocardial arrhythmic after myocardial infarction (MI). In vitro, the cardiomyocytes were subjected to hypoxia (94% N2/5% CO2/1% O2) for 3 hours. Cardiomyocyte apoptosis was assessed by TUNEL staining and western blotting. Urolithin B was found to decrease the number of apoptotic cells after hypoxia. Moreover, there was a substantial decrease in the expression of neural remodeling markers in the Urolithin B treatment group. Urolithin B significantly increased the expression level of gap junction channel protein. Mechanistically, Urolithin B inhibited cardiomyocyte apoptosis by activating Akt/the mammalian target of rapamycin (mTOR) pathway, and the protection of Urolithin B against cardiomyocyte apoptosis was compromised with Akt gene silencing. Furthermore, Urolithin B suppressed nuclear translocation of nuclear factor-kB (NF-κB) to facilitate nerve remodeling. Taken together, our findings suggested that UB reduced the occurrence of myocardial arrhythmias after hypoxia via regulation of the Akt/mTOR pathway and NF-κB nuclear translocation, which highlights the potential of UB as a novel therapy for ischemic heart disease.