Nothofagin

Nothofagin
Product Name Nothofagin
CAS No.: 11023-94-2
Catalog No.: CFN92888
Molecular Formula: C21H24O10
Molecular Weight: 436.4 g/mol
Purity: >=98%
Type of Compound: Chalcones
Physical Desc.: Powder
Targets: TNF-α | IL Receptor | ERK | p38MAPK | JNK | NF-kB | ROS
Source: The heartwoods of Nothofagus fusca
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Price:
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.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
  • Anticancer Res.2014 Jul;34(7):3505-9.
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    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.
    METHODS AND RESULTS:
    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).
    CONCLUSIONS:
    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.
    METHODS AND RESULTS:
    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.
    CONCLUSIONS:
    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.
    METHODS AND RESULTS:
    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.
    CONCLUSIONS:
    Collectively, Asp and Nothofagin possesses antithrombotic activities and offers a basis for development of a novel anticoagulant.
    Inflammation. 2015 Feb 6.
    Anti-inflammatory Effects of Aspalathin and Nothofagin from Rooibos (Aspalathus linearis) In Vitro and In Vivo.[Pubmed: 25655391]
    Aspalathin (Asp) and Nothofagin (Not) are two major active dihydrochalcones found in green rooibos, which have been reported for their anti-oxidant activity.
    METHODS AND RESULTS:
    Here, we investigated the anti-inflammatory effects and underlying mechanisms of Asp and Nothofagin against lipopolysaccharide (LPS)-mediated vascular inflammatory responses. The anti-inflammatory activities of Asp and Nothofagin were determined by measuring permeability, monocytes adhesion and migration, and activation of pro-inflammatory proteins in LPS-activated human umbilical vein endothelial cells (HUVECs) and mice. We found that each compound inhibited LPS-induced barrier disruption, expression of cell adhesion molecules (CAMs), and adhesion/transendothelial migration of neutrophils to human endothelial cells. Asp and Nothofagin also suppressed LPS-induced hyperpermeability and leukocyte migration in vivo. Furthermore, each compound suppressed the production of tumor necrosis factor-α (TNF-α) or interleukin (IL)-6 and the activation of nuclear factor-κB (NF-κB) or extracellular regulated kinases (ERK) 1/2 by LPS. Moreover, treatment with each compound resulted in reduced LPS-induced lethal endotoxemia.
    CONCLUSIONS:
    These results suggest that Asp and Nothofagin posses anti-inflammatory functions by inhibiting hyperpermeability, expression of CAMs, and adhesion and migration of leukocytes, thereby endorsing its usefulness as a therapy for vascular inflammatory diseases.
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