Isofraxidin
(Synonyms: 异嗪皮啶) 目录号 : GC39134
Isofraxidin (6,8-Dimethoxyumbelliferone), a bioactive coumarin compound isolated from the functional foods Siberian ginseng and Apium graveolens, is an anti-bacterial, anti-oxidant, and anti-inflammatory agent.
Cas No.:486-21-5
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
Isofraxidin (6,8-Dimethoxyumbelliferone), a bioactive coumarin compound isolated from the functional foods Siberian ginseng and Apium graveolens, is an anti-bacterial, anti-oxidant, and anti-inflammatory agent.
| Cas No. | 486-21-5 | SDF | |
| 别名 | 异嗪皮啶 | ||
| Canonical SMILES | O=C1C=CC2=CC(OC)=C(O)C(OC)=C2O1 | ||
| 分子式 | C11H10O5 | 分子量 | 222.19 |
| 溶解度 | DMSO: 250 mg/mL (1125.16 mM) | 储存条件 | Store at -20°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 | 4.5007 mL | 22.5033 mL | 45.0065 mL |
| 5 mM | 0.9001 mL | 4.5007 mL | 9.0013 mL |
| 10 mM | 0.4501 mL | 2.2503 mL | 4.5007 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。
Isofraxidin: Synthesis, Biosynthesis, Isolation, Pharmacokinetic and Pharmacological Properties
Molecules 2020 Apr 27;25(9):2040.PMID:32349420DOI:10.3390/molecules25092040.
Isofraxidin (7-hydroxy-6, 8-dimethoxy coumarin) (IF) is a hydroxy coumarin with several biological and pharmacological activities. The plant kingdom is of the most prominent sources of IF, which, among them, Eleutherococcus and Fraxinus are the well-known genera in which IF could be isolated/extracted from their species. Considering the complex pathophysiological mechanisms behind some diseases (e.g., cancer, neurodegenerative diseases, and heart diseases), introducing IF as a potent multi-target agent, which possesses several herbal sources and the multiple methods for isolation/purification/synthesis, along with the unique pharmacokinetic profile and low levels of side effects, could be of great importance. Accordingly, a comprehensive review was done without time limitations until February 2020. IF extraction methods include microwave, mechanochemical, and ultrasound, along with other conventional methods in the presence of semi-polar solvents such as ethyl acetate (EtOAc). In addition to the isolation methods, related synthesis protocols of IF is also of great importance. From the synthesis point of view, benzaldehyde derivatives are widely used as precursors for IF synthesis. Along with the methods of isolation and biosynthesis, IF pharmacokinetic studies showed hopeful in vivo results of its rapid absorption after oral uses, leading to different pharmacological effects. In this regard, IF targets varieties of inflammatory mediators including nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), tumor necrosis factor-α (TNF-α), and matrix metalloproteinases (MMPs). thereby indicating anticancer, cardioprotective, and neuroprotective effects. This is the first review on the synthesis, biosynthesis, isolation, and pharmacokinetic and pharmacological properties of IF in combating different diseases.
Isofraxidin Alleviates Myocardial Infarction Through NLRP3 Inflammasome Inhibition
Inflammation 2020 Apr;43(2):712-721.PMID:31916051DOI:10.1007/s10753-019-01158-z.
Isofraxidin is a well-known coumarin compound refined from traditional Chinese medicines. It has been previously demonstrated to play an anti-inflammatory role in various inflammatory conditions. However, the effect of Isofraxidin on myocardial infarction (MI) remains uncovered. In this study, we aimed to investigate the effect of Isofraxidin on MI. MI mice was created and triphenyltetrazolium chloride (TTC) staining as well as echocardiographic evaluation were conducted to analyze the severity of MI. Oxygen-glucose deprivation (OGD) was used for the mimics of ischemic stress in murine cardiomyocytes, and Cell Counting Kit-8 (CCK-8), Annexin V, and lactate dehydrogenase (LDH) release assays were conducted for cell viability. Western blot was used for the detection of NOD-like receptor family, pyrin domain containing 3 (NLRP3), and adapter protein apoptosis-associated speck-like protein (ASC) in heart tissues and cardiomyocytes. Real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA) were applied for the detection of proinflammatory cytokines. We found that Isofraxidin alleviated the severity of MI and produced a cardio-protective effect against OGD damage. Isofraxidin also decreased the overall and local inflammatory reaction in MI. Those effects were through the inhibition of the NLRP3 inflammasome. Taken together, we initially reported the cardio-protective and alleviative effect of Isofraxidin on MI and uncovered its underlying mechanism related to the NLRP3 inflammasome inhibition.
Suppressive Effects of Isofraxidin on Depressive-like Behaviors Induced by Chronic Unpredictable Mild Stress in Mice
Brain Sci 2022 Oct 11;12(10):1376.PMID:36291310DOI:10.3390/brainsci12101376.
Isofraxidin is an active component of several traditional and functional plants that have beneficial properties for neurodegenerative diseases. In this study, we examined whether Isofraxidin exhibited antidepressant-like effects in chronic unpredictable mild stress (CUMS)-induced mice. Firstly, Isofraxidin could reverse CUMS-induced decrease in body weight gain in mice. Additionally, in the sucrose preference test (SPT), Isofraxidin reversed the decrease in sucrose consumption due to CUMS-induced depressive-like behavior. Isofraxidin also increased locomotor activity in the open field test (OFT) and alleviated immobility duration in the forced swimming test (FST) and tail-suspension test (TST). Furthermore, Isofraxidin decreased levels of corticosterone (CORT), adrenocorticotropic hormone (ACTH), and hypothalamus corticotrophin-releasing hormone (CRH) in the serum after CUMS-induced hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis. Also, Isofraxidin suppresses tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 expression in the hippocampus of CUMS mice. Further investigations demonstrated that Isofraxidin inhibited CUMS-induced activation of nuclear factor kappa B (NF-κB) and NOD-like receptor protein 3 (NLRP3) inflammasomes in the hippocampus. Summarily, in CUMS-induced mice, Isofraxidin reduced depressive-like behaviors, accompanied by its inhibitory effects on hyperactivity of the HPA axis and NF-κB /NLRP3 inflammasomes pathways.
Isofraxidin attenuates IL-1β-induced inflammatory response in human nucleus pulposus cells
J Cell Biochem 2019 Aug;120(8):13302-13309.PMID:30891836DOI:10.1002/jcb.28604.
Inflammation has been demonstrated to be the key factor for intervertebral disc degeneration (IVD), which remains a major public health problem. Isofraxidin is a coumarin compound that possesses strong anti-inflammatory activity. However, the role of Isofraxidin in IVD remains unclear. The aim of this study was to evaluate the effects of Isofraxidin on inflammatory response in human nucleus pulposus cells (NPCs) exposed to interleukin-1β (IL-1β). The results proved that Isofraxidin attenuated the IL-1β-induced significant increases in inflammatory mediators and cytokines including nitric oxide (NO), inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-α), and IL-6. Besides, Isofraxidin also inhibited the induction effect of IL-1β on matrix metalloproteinases (MMP)-3 and MMP-13. Moreover, the NF-κB activation caused by IL-1β was significantly inhibited by Isofraxidin treatment. These findings suggested that Isofraxidin alleviates IL-1β-induced inflammation in NPCs. Our work provided an idea that Isofraxidin might act as a novel preventive role in IVD.
Protective effects of Isofraxidin against scopolamine-induced cognitive and memory impairments in mice involve modulation of the BDNF-CREB-ERK signaling pathway
Metab Brain Dis 2022 Dec;37(8):2751-2762.PMID:35921056DOI:10.1007/s11011-022-00980-z.
Background: Isofraxidin is a coumarin compound mainly isolated from several traditional and functional edible plants beneficial for neurodegenerative diseases, including Sarcandra glabra and Apium graveolens, and Siberian Ginseng. Objective: This study aimed to assess effects of Isofraxidin against memory impairments and cognition deficits in a scopolamine-induced mouse model. Materials & methods: Animals were randomly divided into 6 groups, control, vehicle, donepezil (10 mg/kg, p.o.), and Isofraxidin (3, 10, and 30 mg/kg, p.o.). Isofraxidin or donepezil was administered for 44 days, once per day. The scopolamine insults (1 mg/kg, i.p.) was given from the 21st day, once per day. Morris water maze test and Y-maze test were used for the behavioral test. After that, brain samples were collected for analysis. Results: Firstly, Isofraxidin significantly improved scopolamine-induced behavioral impairments and cognition deficits in Morris water maze and Y-maze test. Then, Isofraxidin facilitated cholinergic activity via inhibiting acetylcholinesterase (AChE) activity. Besides, Isofraxidin decreased lipid peroxidation level but enhanced levels of glutathione, glutathione peroxidase, and superoxide dismutase. Moreover, Isofraxidin suppressed the expression of inflammatory mediators and cytokines. Further investigations showed that Isofraxidin up-regulated expression of brain-derived neurotrophic factor (BDNF), and promoted phosphorylation of tropomyosin-related kinase B (TrkB), cyclic AMP-response element-binding protein (CREB), and extracellular signal-regulated kinase (ERK). Discussion & conclusions: These results suggested that Isofraxidin ameliorated scopolamine-induced cognitive and memory impairments, possibly through regulating AChE activity, suppressing oxidative stress and inflammatory response, and modulating BDNF-CREB-ERK pathways.