Isoquercetin
(Synonyms: 槲皮素-3-葡萄糖苷; Quercetin 3-glucoside) 目录号 : GC41273
A flavonoid with diverse biological activities
Cas No.:482-35-9
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
Isoquercetin (Quercetin 3-glucoside) is a naturally occurring polyphenol that has antioxidant, anti-proliferative, and anti-inflammatory properties. Isoquercetin alleviates ethanol-induced hepatotoxicity, oxidative stress, and inflammatory responses via the Nrf2/ARE antioxidant signaling pathway[1]. Isoquercetin regulates the expression of nitric oxide synthase 2 (NO2) via modulating the nuclear factor-κB (NF-κB) transcription regulation system. Isoquercetin has high bioavailability and low toxicity, is a promising candidate agent to prevent birth defects in diabetic pregnancies[2].
Isoquercetin (Quercetin 3-glucoside; 5-20 μM; 24 hours) substantially reduces ethanol-induced cytotoxicity , protects hepatic cells against ethanol-stimulated liver injury[1].Isoquercetin (10 μM; pre-treat 1 hour) dramatically downregulates the levels of ethanol-induced iNOS protein expression in HepG2 cells[1].
References:
[1]. Lee S, et al. Relative protective activities of quercetin, quercetin-3-glucoside, and rutin in alcohol-induced liver injury. J Food Biochem. 2019 Aug 5:e13002.
[2]. Tan C, et al. Modulation of nuclear factor-κB signaling and reduction of neural tube defects by quercetin-3-glucoside in embryos of diabetic mice. Am J Obstet Gynecol. 2018 Aug;219(2):197.e1-197.e8.
| Cas No. | 482-35-9 | SDF | |
| 别名 | 槲皮素-3-葡萄糖苷; Quercetin 3-glucoside | ||
| Canonical SMILES | OC1=CC(O)=C(C(C(O[C@H]2[C@H](O)[C@@H](O)[C@H](O)[C@@H](CO)O2)=C(C3=CC=C(O)C(O)=C3)O4)=O)C4=C1 | ||
| 分子式 | C21H20O12 | 分子量 | 464.4 |
| 溶解度 | DMF: 10 mg/ml,DMSO: 10 mg/ml,PBS (pH 7.2): 0.3 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 | 2.1533 mL | 10.7666 mL | 21.5332 mL |
| 5 mM | 0.4307 mL | 2.1533 mL | 4.3066 mL |
| 10 mM | 0.2153 mL | 1.0767 mL | 2.1533 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。
Isoquercetin as an Anti-Covid-19 Medication: A Potential to Realize
Front Pharmacol 2022 Mar 2;13:830205.PMID:35308240DOI:10.3389/fphar.2022.830205.
Isoquercetin and quercetin are secondary metabolites found in a variety of plants, including edible ones. Isoquercetin is a monoglycosylated derivative of quercetin. When ingested, Isoquercetin accumulates more than quercetin in the intestinal mucosa where it is converted to quercetin; the latter is absorbed into enterocytes, transported to the liver, released in circulation, and distributed to tissues, mostly as metabolic conjugates. Physiologically, Isoquercetin and quercetin exhibit antioxidant, anti-inflammatory, immuno-modulatory, and anticoagulant activities. Generally Isoquercetin is less active than quercetin in vitro and ex vivo, whereas it is equally or more active in vivo, suggesting that it is primarily a more absorbable precursor to quercetin, providing more favorable pharmacokinetics to the latter. Isoquercetin, like quercetin, has shown broad-spectrum antiviral activities, significantly reducing cell infection by influenza, Zika, Ebola, dengue viruses among others. This ability, together with their other physiological properties and their safety profile, has led to the proposition that administration of these flavonols could prevent infection by severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2), or arrest the progression to severity and lethality of resulting coronavirus disease of 2019 (Covid-19). In silico screening of small molecules for binding affinity to proteins involved SARS-CoV-2 life cycle has repeatedly situated quercetin and Isoquercetin near to top of the list of likely effectors. If experiments in cells and animals confirm these predictions, this will provide additional justifications for the conduct of clinical trials to evaluate the prophylactic and therapeutic efficacy of these flavonols in Covid-19.
Isoquercetin alleviates sleep deprivation dependent hippocampal neurons damage by suppressing NLRP3-induced pyroptosis
Immunopharmacol Immunotoxicol 2022 Oct;44(5):766-772.PMID:35620829DOI:10.1080/08923973.2022.2082976.
Purpose: Sleep deprivation (SD) leads to memory and cognitive impairment due to damage to the hippocampus. Isoquercetin possesses neuron-protective properties. Our study aimed to investigate the effects of Isoquercetin on SD-induced hippocampal neurons damage and the underlying mechanism.Materials and methods: Herein, the cognitive competence was evaluated by Morris water maze test after SD. The morphology of the hippocampus was observed after Nissl staining. Moreover, the level of NLRP3 was detected by Immunofluorescent staining and western blot. In vitro study, pyroptosis was tested by TUNEL assay and flow cytometry. The levels of pyroptosis-related factors were measured by western blot.Results: The results indicated that Isoquercetin improved spatial memory and prevented change of hippocampal neurons of SD mice. Moreover, SD upregulated NLRP3 level, which was downregulated by Isoquercetin. Additionally, Isoquercetin rescued the increase of pyroptosis and the upregulation of NLRP3, caspase-1, ASC, IL-1β, IL-18, and GSDMD levels induced by LPS.Conclusions: In conclusion, Isoquercetin improved learning and cognitive capability of SD mice via suppressing NLRP3-induced pyroptosis of hippocampal neurons cells, suggesting that Isoquercetin might be an efficacious drug for memory disorders caused by SD.
Isoquercetin ameliorated hypoxia/reoxygenation-induced H9C2 cardiomyocyte apoptosis via a mitochondrial-dependent pathway
Biomed Pharmacother 2017 Nov;95:938-943.PMID:28915535DOI:10.1016/j.biopha.2017.08.128.
Isoquercetin exerts multiple pharmacological effects against various diseases. The present research sought to further investigate the role of Isoquercetin in hypoxia/reoxygenation (H/R)-treated cardiomyocytes and its potential mechanism involved. The H/R model in H9C2 cells was established to mimic myocardial I/R injury in vitro. Cell proliferation and apoptosis were tested using MTT assay and Annexin V FITC-PI staining assay, respectively. We found that Isoquercetin protected H9C2 cells from H/R-induced injury as the evidences that Isoquercetin administration attenuated the effects of H/R treatment on H9C2 cell viability, cell apoptosis and ROS generation after H/R treatment. More importantly, Isoquercetin protects mitochondrial function and prevents cytochrome c release in H9C2 cells after I/R injury. In conclusion, these results revealed the potential cardiovascular protective effects of Isoquercetin in the treatment of I/R-related myocardial injury.
Isoquercetin Improves Inflammatory Response in Rats Following Ischemic Stroke
Front Neurosci 2021 Feb 9;15:555543.PMID:33633530DOI:10.3389/fnins.2021.555543.
Inflammatory response contributes to brain injury after ischemia and reperfusion (I/R). Our previous literature has shown Isoquercetin plays an important role in protecting against cerebral I/R injury. The present study was conducted to further investigate the effect of Isoquercetin on inflammation-induced neuronal injury in I/R rats with the involvement of cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) and inhibitor of NF-κB (I-κB)/nuclear factor-kappa B (NF-κB) signaling pathway mediated by Toll-like receptor 4 (TLR4) and C5a receptor 1 (C5aR1). In vivo middle cerebral artery occlusion and reperfusion (MCAO/R) rat model and in vitro oxygen-glucose deprivation and reperfusion (OGD/R) neuron model were used. MCAO/R induced neurological deficits, cell apoptosis, and release of cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 in ischemic brain in rats. Simultaneously, the expression of TLR4 and C5aR1 was significantly up-regulated in both MCAO/R rats and OGD/R neurons, accompanied with the inhibition of cAMP/PKA signaling and activation of I-κB/NF-κB signaling in the cortex of MCAO/R rats. Over-expression of C5aR1 in neurons induced decrease of cell viability, exerting similar effects with OGD/R injury. Isoquercetin acted as a neuroprotective agent against I/R brain injury to suppress inflammatory response and improve cell recovery by inhibiting TLR4 and C5aR1 expression, promoting cAMP/PKA activation, and inhibiting I-κB/NF-κB activation and Caspase 3 expression. TLR4 and C5aR1 contributed to inflammation and apoptosis via activating cAMP/PKA/I-κB/NF-κB signaling during cerebral I/R, suggesting that this signaling pathway may be a potent therapeutic target in ischemic stroke. Isoquercetin was identified as a neuroprotective agent, which maybe a promising therapeutic agent used for the treatment of ischemic stroke and related diseases.
Neuroprotective Effects of Isoquercetin: An In Vitro and In Vivo Study
Cell J 2021 Aug;23(3):355-365.PMID:34308580DOI:10.22074/cellj.2021.7116.
Objective: Alzheimer's disease (AD) is considered a neurodegenerative disease that affects the cognitive function of elderly individuals. In this study, we aimed to analyze the neuroprotective potential of Isoquercetin against the in vitro and in vivo models of AD and investigated the possible underlying mechanisms. Materials and methods: The experimental study was performed on PC12 cells treated with lipopolysaccharide (LPS). Reactive oxygen species (ROS), antioxidant parameters, and pro-inflammatory cytokines were measured. In an in vivo approach, Wistar rats were used and divided into different groups. We carried out the Morris water test to determine the cognitive function. Biochemical parameters, antioxidant parameters, and pro-inflammatory parameters were examined. Results: The non-toxic effect on PC12 cells was shown by Isoquercetin. Isoquercetin significantly reduced the production of nitrate and ROS, along with the altered levels of antioxidants. Isoquercetin significantly (P<0.001) down-regulated proinflammatory cytokines in PC12 cells treated with LPS. In the in vivo approach, isoquercetintreated groups considerably showed the up-regulation in the latency and transfer latency time, as compared with AD groups. Isoquercetin significantly reduced Aβ-peptide, protein carbonyl, while enhanced the production of brainderived neurotrophic factor (BDNF) and acetylcholinesterase (AChE). Isoquercetin significantly (P<0.001) reduced pro-inflammatory cytokines and inflammatory mediators, as compared with AD groups. Conclusion: Based on the results, we may infer that, through antioxidant and anti-inflammatory systems, Isoquercetin prevented neurochemical and neurobehavioral modifications against the model of colchicine-induced AD rats.