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  • Nothofagin


    产品编号 CFN92888
    CAS编号 11023-94-2
    分子式 = 分子量 C21H24O10 = 436.4
    产品纯度 >=98%
    物理属性 Powder
    化合物类型 Chalcones
    植物来源 The heartwoods of Nothofagus fusca
    产品名称 产品编号 CAS编号 包装 QQ客服
    Nothofagin CFN92888 11023-94-2 1mg QQ客服:2159513211
    Nothofagin CFN92888 11023-94-2 5mg QQ客服:2159513211
    Nothofagin CFN92888 11023-94-2 10mg QQ客服:2159513211
    Nothofagin CFN92888 11023-94-2 20mg QQ客服:2159513211
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  • 生物活性
    Description: Nothofagin has antioxidant, and antithrombotic activities, it possesses anti-inflammatory activity by inhibiting hyperpermeability, expression of CAMs, and adhesion and migration of leukocytes, thereby endorsing its usefulness as a therapy for vascular inflammatory diseases. Nothofagin may have significant benefits in the treatment of diabetic complications. Nothofagin has potential to as an anti-sendothelial cell protein C receptor shedding reagent against phorbol-12-myristate 13-acetate and cecal ligation and puncture -mediated endothelial cell protein C receptor shedding.
    Targets: TNF-α | IL Receptor | ERK | p38MAPK | JNK | NF-kB | ROS
    In vitro:
    Fitoterapia. 2015 Jan;100:179-86.
    Aspalathin and nothofagin from rooibos (Aspalathus linearis) inhibit endothelial protein C receptor shedding in vitro and in vivo.[Pubmed: 25510322]
    Aspalathin (Asp) and Nothofagin (Not) are two major active dihydrochalcones found in green rooibos, which have been reported for their anti-oxidant activity.
    Increasing evidence has demonstrated that beyond its role in the activation of protein C, endothelial cell protein C receptor (EPCR) is also involved in vascular inflammation. EPCR activity is markedly changed by ectodomain cleavage and its release as the soluble EPCR. EPCR can be shed from the cell surface, which is mediated by tumor necrosis factor-α converting enzyme (TACE). However, little is known about the effects of Asp and Nothofagin on EPCR shedding. Our results demonstrated that Asp and Nothofagin induced potent inhibition of phorbol-12-myristate 13-acetate (PMA)-, tumor necrosis factor (TNF)-α-, interleukin (IL)-1β, and cecal ligation and puncture (CLP)-induced EPCR shedding. Asp and Nothofagin also inhibited the expression and activity of PMA-induced TACE in endothelial cells. Asp and Nothofagin also suppressed CLP-induced protein C decrease in mice and thrombin generation in HUVECs. In addition, treatment with Asp and Nothofagin resulted in reduced PMA-stimulated phosphorylation of p38, extracellular regulated kinase (ERK) 1/2, and c-Jun N-terminal kinase (JNK).
    These results demonstrate the potential of Asp and Nothofagin as an anti-sEPCR shedding reagent against PMA and CLP-mediated EPCR shedding.
    Inflammation. 2015 Feb;38(1):445-55.
    Aspalathin and Nothofagin from Rooibos (Aspalathus linearis) inhibits high glucose-induced inflammation in vitro and in vivo.[Pubmed: 25338943]
    Vascular inflammation plays a key role in the initiation and progression of atherosclerosis, a major complication of diabetes mellitus. Aspalathin (Asp) and Nothofagin (Not) are two major active dihydrochalcones found in green rooibos, which have been reported for their antioxidant activity.
    In this study, we assessed whether Asp or Nothofagin can suppress vascular inflammation induced by high glucose (HG) in human umbilical vein endothelial cells (HUVECs) and mice. We monitored the effects of Asp or Nothofagin on HG-induced vascular hyperpermeability, expression of cell adhesion molecules (CAMs), formation of reactive oxygen species (ROS), and activation of nuclear factor (NF)-κB in vitro and in vivo.
    Our data indicate that HG markedly increased vascular permeability, monocyte adhesion, expression of CAMs, formation of ROS, and activation of NF-κB. Remarkably, treatment of Asp or Nothofagin inhibited HG-mediated vascular hyperpermeability, adhesion of monocytes toward HUVECs, and expression of CAMs. In addition, Asp or Nothofagin suppressed the formation of ROS and the activation of NF-κB. Since vascular inflammation induced by HG is critical in the development of diabetic complications, our results suggest that Asp or Nothofagin may have significant benefits in the treatment of diabetic complications.
    Arch Pharm Res. 2014 Oct 18.
    Antithrombotic activities of aspalathin and nothofagin via inhibiting platelet aggregation and FIIa/FXa.[Pubmed: 25325928]
    Aspalathin (Asp) and Nothofagin (Not) are two major active dihydrochalcones found in green rooibos tea (Aspalathus linearis; family, Fabaceae; tribe, Crotalarieae), which have been reported for their anti-oxidant activity.
    Here, the anticoagulant activities of Asp and Nothofagin were examined by monitoring activated partial thromboplastin time (aPTT), prothrombin time (PT), and the activities of thrombin (Factor IIa, FIIa) and activated factor X (FXa). And, the effects of Asp and Nothofagin on expression of plasminogen activator inhibitor type 1 (PAI-1) and tissue-type plasminogen activator (t-PA) were evaluated in tumor necrosis factor (TNF)-α activated human umbilical vein endothelial cells (HUVECs). Treatment with Asp and Nothofagin resulted in prolonged aPTT and PT and inhibition of the activities of thrombin and FXa, as well as inhibited production of thrombin and FXa in HUVECs. In addition, Asp and Nothofagin inhibited thrombin-catalyzed fibrin polymerization and platelet aggregation. Asp and Nothofagin also elicited anticoagulant effects in mice. In addition, treatment with Asp and Nothofagin resulted in significant reduction of the PAI-1 to t-PA ratio.
    Collectively, Asp and Nothofagin possesses antithrombotic activities and offers a basis for development of a novel anticoagulant.
    Chem Biol Interact . 2019 Jan 25;298:1-7.
    Nothofagin suppresses mast cell-mediated allergic inflammation[Pubmed: 30392763]
    Abstract Mast cells play a major role in immunoglobulin E-mediated allergic inflammation, which is involved in asthma, atopic dermatitis, and allergic rhinitis. Nothofagin has been shown to ameliorate various inflammatory responses such as the septic response and vascular inflammation. In this study, we assessed the inhibitory effect of nothofagin on allergic inflammation using cultured/isolated mast cells and an anaphylaxis mouse model. Nothofagin treatment prevented histamine and β-hexosaminidase release by reducing the influx of calcium into the cytosol in a concentration-dependent manner. Nothofagin also inhibited the gene expression and secretion of pro-inflammatory cytokines such as tumor necrosis factor-α and interleukin-4 by downregulating the phosphorylation of Lyn, Syk, Akt and nuclear translocation of nuclear factor-κB. To confirm these effects of nothofagin in vivo, we used a passive cutaneous anaphylaxis mouse model. Topical administration of nothofagin suppressed local pigmentation and ear thickness. Taken together, these results suggest nothofagin as a potential candidate for the treatment of mast cell-involved allergic inflammatory diseases. Keywords: Allergic inflammation; Histamine; Mast cells; Nothofagin.
    In vivo:
    Chem Biol Interact . 2018 Jan 5;279:227-233.
    Prolonged diuretic and saluretic effect of nothofagin isolated from Leandra dasytricha (A. Gray) Cogn. leaves in normotensive and hypertensive rats: Role of antioxidant system and renal protection[Pubmed: 29198636]
    Abstract Although the acute diuretic effect of nothofagin has been recently demonstrated, its effects after dose-repeated treatment have not yet been explored. For that, male Wistar normotensive (NTR) and spontaneously hypertensive rats (SHR) were orally treated, once a day, with vehicle (VEH: distilled water; 1 ml/kg), hydrochlorothiazide (HCTZ; 10 mg/kg) or nothofagin (NOT; 1 mg/kg). The cumulative diuretic index and urinary electrolytes excretion were measured each 24 h. On the last day of the experiment (7th day), urine, blood and kidney samples were collected for biochemical and molecular analyzes. The urinary volume of both NTR and SHR were significantly increased with the treatment with NOT (from the second to the seventh day of treatment), with final values reaching an increase of 56% and 82%, respectively, when compared with VEH-treated group. This effect was associated with increased levels of urinary excretion of Na+ and Cl-, without any changes on K+ excretion. None of the treatments modified urinary pH or density values. Importantly, neither the NOT nor the HCTZ caused any change in body weight following the dose-repeated treatment, and also did not provoke an electrolytic disturbance. Regarding the renal analyzes, when compared with the vehicle-treated NTR group, the activity of superoxide dismutase (SOD) and the reduced glutathione (GSH) levels in kidney homogenates of the SHR group were decreased, while the generation of lipid hydroperoxides were significantly increased. The daily treatment with NOT was able to restore the GSH levels and SOD activity, as well as reduced the lipoperoxidation in the kidney homogenates obtained from SHR animals. Finally, NOT significantly augmented the levels of nitrite, a marker of nitric oxide production, in the plasma obtained from SHR group when compared with the vehicle-treated only NTR. This study revealed the prolonged diuretic and saluretic effect of nothofagin in normotensive and hypertensive rats. Our data also showed the renal protective effects of nothofagin by the improvement of antioxidative capacity, as well as by the augmented bioavailability of plasma nitric oxide in the hypertensive group. Keywords: Antioxidant; Diuresis; Glutathione; Lipoperoxidation; Nitric oxide; Superoxide dismutase.
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 2.2915 mL 11.4574 mL 22.9148 mL 45.8295 mL 57.2869 mL
    5 mM 0.4583 mL 2.2915 mL 4.583 mL 9.1659 mL 11.4574 mL
    10 mM 0.2291 mL 1.1457 mL 2.2915 mL 4.583 mL 5.7287 mL
    50 mM 0.0458 mL 0.2291 mL 0.4583 mL 0.9166 mL 1.1457 mL
    100 mM 0.0229 mL 0.1146 mL 0.2291 mL 0.4583 mL 0.5729 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    产品名称 产品编号 CAS编号 分子式 = 分子量 位单 联系QQ
    三叶甙; Trilobatin CFN98658 4192-90-9 C21H24O10 = 436.4 20mg QQ客服:1413575084
    三叶甙2''-乙酸酯; Trilobatin 2''-acetate CFN97111 647853-82-5 C23H26O11 = 478.5 5mg QQ客服:2056216494
    Nothofagin; Nothofagin CFN92888 11023-94-2 C21H24O10 = 436.4 5mg QQ客服:215959384
    根皮素-3',5'-二-C-β-葡萄糖苷; Phloretin 3',5'-Di-C-glucoside CFN95306 357401-40-2 C27H34O15 = 598.2 10mg QQ客服:1413575084
    柚皮苷二氢查尔酮; Naringin dihydrochalcone CFN90437 18916-17-1 C27H34O14 = 582.55 20mg QQ客服:3257982914
    3-羟基根皮苷; Sieboldin CFN70294 18777-73-6 C21H24O11 = 452.4 5mg QQ客服:1413575084
    新橙皮苷二氢查尔酮; Neosperidin dihydrochalcone CFN98168 20702-77-6 C28H36O15 = 612.58 20mg QQ客服:2159513211
    橙皮苷甲基查尔酮; Hesperidin methylchalcone CFN80405 24292-52-2 C29H36O15 = 624.59 20mg QQ客服:1413575084
    地奥司明杂质5; Diosmin Impurity 5 CFN95311 122087-66-5 C30H38O15 = 638.6 10mg QQ客服:1413575084
    二氢马里苷; Dihydromarein CFN90853 N/A C21H24O11 = 452.4 5mg QQ客服:2056216494





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