Hesperidin methylchalcone
(Synonyms: 甲基橙皮甙查尔酮) 目录号 : GC60897
Hesperidin methylchalcone is the Citrus original products with powerful antioxidant activity.
Cas No.:24292-52-2
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
Hesperidin methylchalcone is the Citrus original products with powerful antioxidant activity.
| Cas No. | 24292-52-2 | SDF | |
| 别名 | 甲基橙皮甙查尔酮 | ||
| Canonical SMILES | COC1=C(C(/C=C/C2=CC(O)=C(OC)C=C2)=O)C(O)=CC(O[C@H](O3)[C@H](O)[C@@H](O)[C@H](O)[C@H]3CO[C@@H]4O[C@@H](C)[C@H](O)[C@@H](O)[C@H]4O)=C1 | ||
| 分子式 | C29H36O15 | 分子量 | 624.59 |
| 溶解度 | DMSO: 50 mg/mL (80.05 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 | 1.6011 mL | 8.0053 mL | 16.0105 mL |
| 5 mM | 0.3202 mL | 1.6011 mL | 3.2021 mL |
| 10 mM | 0.1601 mL | 0.8005 mL | 1.6011 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。
Hesperidin methylchalcone Suppresses Experimental Gout Arthritis in Mice by Inhibiting NF-κB Activation
J Agric Food Chem 2018 Jun 27;66(25):6269-6280.PMID:29852732DOI:10.1021/acs.jafc.8b00959.
Gout arthritis is a painful inflammatory disease induced by monosodium urate (MSU) crystals. We evaluate the therapeutic potential of the flavonoid Hesperidin methylchalcone (HMC) in a mouse model of gout arthritis induced by intra-articular injection of MSU (100 μg/10 μL). Orally given HMC (3-30 mg/kg, 100 μL) reduced in a dose-dependent manner the MSU-induced hyperalgesia (44%, p < 0.05), edema (54%, p < 0.05), and leukocyte infiltration (70%, p < 0.05). HMC (30 mg/kg) inhibited MSU-induced infiltration of LysM-eGFP+ cells (81%, p < 0.05), synovitis (76%, p < 0.05), and oxidative stress (increased GSH, FRAP, and ABTS by 62, 78, and 73%, respectively; reduced O2- and NO by 89 and 48%, p < 0.05) and modulated cytokine production (reduced IL-1β, TNF-α, IL-6, and IL-10 by 35, 72, 37, and 46%, respectively, and increased TGF-β by 90%, p < 0.05). HMC also inhibited MSU-induced NF-κB activation (41%, p < 0.05), gp91phox (66%, p < 0.05) and NLRP3 inflammasome components mRNA expression in vivo (72, 77, 71, and 73% for NLRP3, ASC, pro-caspase-1, and pro-IL-1 β, respectively, p < 0.05), and induced Nrf2/HO-1 mRNA expression (3.9- and 5.1-fold increase, respectively, p < 0.05). HMC (30, 100, and 300 μM) did not inhibit IL-1β secretion by macrophages primed by LPS and challenged with MSU (450 μg/mL), demonstrating that the anti-inflammatory effect of HMC in gout arthritis depends on inhibiting NF-κB but not on direct inhibition of inflammasome. The pharmacological effects of HMC indicate its therapeutic potential for the treatment of gout.
Hesperidin methylchalcone (HMC) hinders amyloid-β induced Alzheimer's disease by attenuating cholinesterase activity, macromolecular damages, oxidative stress and apoptosis via regulating NF-κB and Nrf2/HO-1 pathways
Int J Biol Macromol 2023 Apr 1;233:123169.PMID:36623626DOI:10.1016/j.ijbiomac.2023.123169.
Phytocompounds therapy has recently emerged as an effective strategy to treat Alzheimer's disease. Herein, the protective effect of Hesperidin methylchalcone (HMC) was evaluated through Alzheimer's disease models of Neuro-2a cells and Wistar rats. The in vitro results showed that HMC possesses significant ability to inhibit the acetylcholinesterase enzyme and exhibiting anti-aggregation and disaggregation properties. Furthermore, HMC could protect the Neuro-2a cells against Aβ-induced neurotoxicity. Simultaneously, HMC treatment significantly improved the cognitive deficits caused by Aβ-peptide on spatial memory in Wistar rats. HMC significantly enhanced the cholinergic effects by inhibiting AChE, BuChE, β-secretase activity, caspase-3 activity, and attenuating macromolecular damages and apoptosis. Notably, HMC reduced the Aβ-induced oxidative stress by activating the antioxidative defence enzymes. In addition, the HMC treatment suppressed the expression of immunocytokines such as p-NF-κB p65, p-IκBα, induced by Aβ; whereas upregulating Nrf2, HO-1 in brain homogenate. These results suggest that HMC could attenuate Aβ-induced neuroinflammation in brain via suppressing NF-κB signalling pathway and activating the Nrf2/HO-1 pathway, thereby improving memory and cognitive impairments in Wistar rats. Overall, the present study reports that HMC can act as a potent candidate with multi-faceted neuroprotective potential against Aβ-induced memory dysfunction in Wistar rats for the treatment of Alzheimer's disease.
Absorption and elimination of (14C) Hesperidin methylchalcone in the rat
Eur J Drug Metab Pharmacokinet 1981;6(3):171-7.PMID:7308237DOI:10.1007/BF03189486.
Hesperidin methylchalcone resorption and excretion were studied in rats, using 14C-labelling. The level of radioactivity in the blood showed a peak 1-2 hours after oral administration of the labelled compound, at a dose of 10 mg/kg body weight. The blood kinetics pattern suggested an entero-hepatic cycle, which was demonstrated by i.v. administration of the compound at the same dose. The blood profiles for both administration routes, demonstrated that the bioavailability of the active principle was good. Urinary excretion was lower than faecal excretion after oral ingestion, and both were comparable after administration via the i.v. route. Moreover, excretion mainly occurred within the first 24 hours following administration. When Hesperidin methylchalcone was given in a therapeutic, pharmaceutical formulation, its bioavailability was greatly improved. (This was not due to the alcoholic ingredient in the formula).
Effect of Ruscus extract and Hesperidin methylchalcone on hypoxia-induced activation of endothelial cells
Int Angiol 1999 Dec;18(4):306-12.PMID:10811519doi
Background: Ruscus aculeatus extract and the flavonoid Hesperidin methylchalcone (HMC) are drugs used in the treatment of chronic venous insufficiency. Methods: In the present study, we investigated their effects on the activation of endothelial cells by hypoxia, a condition which mimics venous blood stasis. Results: We observed that Ruscus extract was able to inhibit the activation of endothelial cells by hypoxia: the decrease in ATP content, the activation of phospholipase A2 as well as the subsequent increase in neutrophil adherence with a maximal protection obtained at 50 microg/ml. HMC was also able to inhibit the hypoxia-induced decrease in ATP content. Furthermore, the effects of Ruscus extract and of HMC on this decrease seem to be additive. Conclusions: The biochemical mechanism evidenced in this work might explain some of the beneficial therapeutic effects of these products in the treatment of chronic venous insufficiency patients.
Clinical and capillaroscopic evaluation in the treatment of chronic venous insufficiency with Ruscus aculeatus, Hesperidin methylchalcone and ascorbic acid in venous insufficiency treatment of ambulatory patients
Int Angiol 2007 Dec;26(4):378-84.PMID:18091707doi
Aim: Clinical and capillaroscopic evaluation of an association of Ruscus aculeatus, Hesperidin methylchalcone (HMC) and ascorbic acid in chronic venous insufficiency Methods: A prospective, multicenter and open clinical study. Chronic venous insufficiency patients were studied using clinical, etiological, anatomical, physiological classification (CEAP) symptom scale. Symptomatology, CEAP scale, and baseline, 2-, 4-, 6- and 8-week skin capillaroscopy were assessed. Treatment consisted of two capsules per day of Ruscus aculeatus 150 mg/HMC 150 mg/ascorbic acid 100 mg during 8 weeks. Results: A total of 124 patients were studied, 109 female (89.28%), with a mean age of 52.5 (33-80+9.8). Initial intense reports were 79% pain, 85% heaviness, 74% cramps, 82% edema, decreasing to 20%, 12%, 8% and 14%, respectively, within two weeks, and symptomatology being absent at the end of treatment. Capillaroscopy changes at treatment completion were: 98% to 20% inter-capillary fluid decrease; 80% to 20% efferent loop thickening; 5% to 2% peri-capillary bed, and 5% to 4% mega-capillaries. Conclusion: Severe symptom decrease started from the second week until there were no symptoms at the end of treatment. It is the first time morphologic changes were observed in chronic venous insufficiency through capillaroscopy following a pharmacological intervention. Capillary-level effect was proportional to symptom decrease. Improvement was seen from the second week of treatment.