Visnagin
(Synonyms: 齿阿米素) 目录号 : GC49168
A furanochromone with diverse biological activities
Cas No.:82-57-5
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
Visnagin is a polyketide synthase-derived furanochromone originally isolated from A. visnaga that has diverse biological activities.1,2,3,4,5 It inhibits the germination and growth of ryegrass (IC50s = 502 and 214 µM, respectively).2 Visnagin (100 µg/ml) is cytotoxic to, and induces apoptosis in, HT-144 melanoma cells.3 It reduces LPS-stimulated increases in the secretion of TNF-α, IL-1β, and IFN-γ in BV-2 microglial cells when used at concentrations of 50 and 100 µM.4 Visnagin (25 mg/kg) protects against cardiomyopathy induced by doxorubicin in mice.5
1.Abe, I.Engineering of plant polyketide biosynthesisChem. Pharm. Bull. (Tokyo)56(11)1505-1514(2008) 2.Travaini, M.L., Sosa, G.M., Ceccarelli, E.A., et al.Khellin and visnagin, furanochromones from Ammi visnaga (L.) Lam., as potential bioherbicidesJ. Agric. Food Chem.64(50)9475-9487(2016) 3.Aydo?mu?-ÖztÜrk, F., Jahan, H., Beyazit, N., et al.The anticancer activity of visnagin, isolated from Ammi visnaga L., against the human malignant melanoma cell lines, HT 144Mol. Biol. Rep.46(2)1709-1714(2019) 4.Lee, J.-K., Jung, J.-S., Park, S.-H., et al.Anti-inflammatory effect of visnagin in lipopolysaccharide-stimulated BV-2 microglial cellsArch. Pharm. Res.33(11)1843-1850(2010) 5.Liu, Y., Asnani, A., Zou, L., et al.Visnagin protects against doxorubicin-induced cardiomyopathy through modulation of mitochondrial malate dehydrogenaseSci. Transl. Med.6(266)266ra170(2014)
| Cas No. | 82-57-5 | SDF | |
| 别名 | 齿阿米素 | ||
| Canonical SMILES | O=C1C=C(C)OC2=C1C(OC)=C3C=COC3=C2 | ||
| 分子式 | C13H10O4 | 分子量 | 230.2 |
| 溶解度 | DMF: 10 mg/ml,DMF:PBS (pH 7.2) (1:5): 0.16 mg/ml,DMSO: 5 mg/ml,Ethanol: 1 mg/ml | 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 | 4.344 mL | 21.7202 mL | 43.4405 mL |
| 5 mM | 0.8688 mL | 4.344 mL | 8.6881 mL |
| 10 mM | 0.4344 mL | 2.172 mL | 4.344 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。
Visnagin ameliorates myocardial ischemia/reperfusion injury through the promotion of autophagy and the inhibition of apoptosis
Eur J Histochem 2020 Sep 7;64(s2):3131.PMID:32909422DOI:10.4081/ejh.2020.3131.
Visnagin is a furanochromone and one of the main compounds of Ammi visnaga L. that had been used to treat nephrolithiasis in Ancient Egypt. Nowadays, Visnagin was widely used to treat angina pectoris, urolithiasis and hypertriglyceridemia. The potential mechanisms of Visnagin involved in inflammation and cardiovascular disease were also identified. But the protective effect of Visnagin on myocardial ischemia/reperfusion injury has not been confirmed. Our aim was, for the first time, to investigate the potential protective effect of Visnagin on cardiac function after myocardial ischemia-reperfusion injury in a rat model, and to identify its underlying mechanism involving the inhibition of apoptosis and induction of autophagy. Thirty SD rats were randomly divided into sham group, ischemia/reperfusion group (IR), ischemia/reperfusion with Visnagin (IR + Visnagin) group. Myocardial ischemia/Reperfusion injury model was established. Hemodynamic measurements and echocardiography were used to analyze cardiac function, TUNEL staining and caspase activity, LC3 dots were detected with immunofluorescence staining, LC3 expression was evaluated by western blot analysis, transmission electron microscopy (TEM) was used to detect autophagosomes. Compared with the sham group and Visnagin group, the cardiac dysfunction, LC3II, autophagy flow in the IR+ Visnagin group increased significantly (P<0.01), but the activity of caspase-3 and caspase-9 and the apoptotic in the IR + Visnagin group decreased significantly (P<0.01). In conclusion, Visnagin may play a protective role in ischemia/reperfusion injury by inducing autophagy and reducing apoptosis.
Visnagin attenuates acute pancreatitis via Nrf2/NFκB pathway and abrogates associated multiple organ dysfunction
Biomed Pharmacother 2019 Apr;112:108629.PMID:30798137DOI:10.1016/j.biopha.2019.108629.
Acute pancreatitis (AP) is an exocrine dysfunction of the pancreas where oxidative stress and inflammatory cytokines play a key role in induction and progression of the disease. Studies have demonstrated that antioxidant phytochemicals have been effective in improving pancreatitis condition, but there are no clinically approved drugs till date. Our study aims to assess the preventive activity of Visnagin, a novel phytochemical isolated from Ammi visnaga against cerulein induced AP. Male Swiss albino mice were divided into six groups (n = 6, each group) comprising of normal control, cerulein control, seven day pre-treatment with Visnagin at three dose levels; Visnagin low dose (10 mg/kg), Visnagin mid dose (30 mg/kg), Visnagin high dose (60 mg/kg) and Visnagin control (60 mg/kg). AP was induced by six injections of cerulein (50 μg/kg, i.p.) on the 7th day and the animals were sacrificed after 6 h of last cerulein dose. Various markers of pancreatic function, oxidative stress and inflammation were assessed. Visnagin was found to be effective in reducing plasma amylase and lipase levels, reduced cerulein induced oxidative stress. Visnagin dose dependently decreased the expression of IL-1β, IL-6, TNF-α and IL-17. It attenuated the levels of nuclear p65-NFκB. Visnagin improved the antioxidant defence by improving Nrf2 expression and halted pancreatic inflammation by suppressing NFκB and nitrotyrosine expression in the acinar cells. Further, it attenuated the expression of markers of multiple organ dysfunction syndrome and reduced inflammatory cytokines in lungs and intestine. Cumulatively, these findings indicate that Visnagin has substantial potential to prevent cerulein induced AP.
Neuroprotective, Anti-inflammatory Effect of Furanochrome, Visnagin Against Middle Cerebral Ischemia-Induced Rat Model
Appl Biochem Biotechnol 2022 Dec;194(12):5767-5780.PMID:35819694DOI:10.1007/s12010-022-04009-0.
In recent years, the medical field had significantly progressed to a greater extent which was evidenced with increased life expectancy and decreased mortality rate. Due to the growth of medical field, numerous communicable diseases are prevented and eradicated, whereas the non-communicable disease incidence has been increased globally. One such non-communicable disease which threatens the global population is stroke. Stroke tends to be the second leading cause of death and disability in older population. In lower- and middle-income countries, increased incidence rate of stroke was also evidenced in younger population which is alarming. Lifestyle changes, poor physical activity, stress, consumption of alcohol, oral contraception, and smoking tend to be the causative agents of stroke. Since thrombus formation is the major pathology of stroke, drugs were targeted to thrombolysis. Currently thrombolytic, antiplatelet, and anticoagulant therapies were given for the stroke patients. But the recovery rate of stroke patients with available drugs is very slow. Hence, it is a need of today to discover a drug with increased recovery rate and decreased or nil side effects. Phytochemicals are the best options to treat such non-communicable chronic diseases. Visnagin is one such compound which is used to regulate blood pressure, treat kidney stones, tumors of bile duct, renal colic, and whooping cough. It possesses anti-inflammatory, neuroprotective, and cardioprotective properties; it was also proven to treat epileptic seizures. In this study, the anti-ischemic effect of a furanochrome Visnagin was assessed in in vivo rat model. Middle cerebral ischemic/reperfusion was induced in healthy male Sprague Dawley rats and treated with different concentrations of Visnagin. The neuroprotective effect of Visnagin against cerebral ischemia-induced rats was assessed by analyzing the neurological score, brain edema, infract volume, and Evans blue leakage. The anti-inflammatory property of Visnagin was assessed by quantifying proinflammatory cytokines in serum and brain tissues of cerebral ischemia-induced rats. Prostaglandin E-2, COX-2, and NFκ-β were estimated to assess the anti-ischemic effect of Visnagin. Histopathological analysis with H&E staining was performed to confirm the neuroprotective effect of Visnagin against cerebral ischemia. Our results authentically confirm that Visnagin has prevented the inflammation in brain region of cerebral ischemia-induced rats. The neurological scoring and the quantification of PGE-2, COX-2, and NFκ-β prove the anti-ischemic effect of Visnagin. Furthermore, the histopathological analysis of hippocampal region provides evidence to the neuroprotective effect of Visnagin against cerebral ischemia. Overall, our study confirms Visnagin as a potent alternative drug to treat stroke.
Neuroprotective effects of Visnagin on cerebral ischemia-reperfusion injury rats and the underlying mechanisms
Eur Rev Med Pharmacol Sci 2022 Jun;26(12):4371-4379.PMID:35776038DOI:10.26355/eurrev_202206_29076.
Objective: Cerebral ischemia-reperfusion (I/R), caused by the treatments of ischemic stroke, usually leads to brain injury. Inflammation, oxidative stress, and autophagy play pivotal roles in the pathology. Visnagin presents a protective effect on I/R injured animal models of the heart, liver, kidney, and other organs. In our research, we identified the neuroprotective effects and the underlying mechanisms of Visnagin in cerebral I/R injured models. Materials and methods: We constructed rat models of cerebral I/R injury and categorized them into 5 groups: sham operation group, I/R model group, and Visnagin treatment I/R group (10, 30, 60 mg/kg). The neurological deficits of the rats were analyzed after 24 hours of reperfusion, then, the contents of glutathione peroxidase, malondialdehyde, superoxide dismutase catalase, caspase-3, nuclear factor kappa-B p65 unit, tumor necrosis factor-α, interleukin-1β, and interleukin6 were measured in rat models. The expressions of Bcl-2 and Bax were detected by Western blot analysis. Results: Our results suggested that the administration of Visnagin alleviated the cognitive dysfunction, reduced the activities of inflammatory factors, promoted the protein expression of Bcl-2, and downregulated the expression of Bax in the I/R injured rat model. Conclusions: Visnagin exerts a neuroprotective effect during I/R injury in rats, the underlying mechanisms may be the effect of attenuating neuroinflammation, anti-oxidative and inhibition of apoptosis.
Coumarins as Modulators of the Keap1/Nrf2/ARE Signaling Pathway
Oxid Med Cell Longev 2020 Apr 22;2020:1675957.PMID:32377290DOI:10.1155/2020/1675957.
The Keap1/Nrf2/ARE system is a central defensive mechanism against oxidative stress which plays a key role in the pathogenesis and progression of many diseases. Nrf2 is a redox-sensitive transcription factor controlling a variety of downstream antioxidant and cytodefensive genes. Nrf2 has a powerful anti-inflammatory activity mediated via modulating NF-κB. Therefore, pharmacological activation of Nrf2 is a promising therapeutic strategy for the treatment/prevention of several diseases that are underlined by both oxidative stress and inflammation. Coumarins are natural products with promising pharmacological activities, including antioxidant, anticancer, antimicrobial, and anti-inflammatory efficacies. Coumarins are found in many plants, fungi, and bacteria and have been widely used as complementary and alternative medicines. Some coumarins have shown an ability to activate Nrf2 signaling in different cells and animal models. The present review compiles the research findings of seventeen coumarin derivatives of plant origin (imperatorin, Visnagin, urolithin B, urolithin A, scopoletin, esculin, esculetin, umbelliferone, fraxetin, fraxin, daphnetin, anomalin, wedelolactone, glycycoumarin, osthole, hydrangenol, and isoimperatorin) as antioxidant and anti-inflammatory agents, emphasizing the role of Nrf2 activation in their pharmacological activities. Additionally, molecular docking simulations were utilized to investigate the potential binding mode of these coumarins with Keap1 as a strategy to disrupt Keap1/Nrf2 protein-protein interaction and activate Nrf2 signaling.