|Source:||The root of Angelica biserrata (Shan et Yuan) Yuan et Shan.|
|Biological Activity or Inhibitors:||1. Nodakenin possesses neuroprotective, antiaggregatory, antibacterial, and memory
2. Nodakenin down-regulates the expression of the proinflammatory iNOS, COX-2, TNF-α, IL-6, and IL-1β genes in macrophages by interfering with the activation of TRAF6, thus preventing NF-κB activation.
3. Nodakenin can inhibit acetylcholinesterase activity in a dose-dependent manner (IC(50)=84.7 microM), it may be a useful for the treatment of cognitive impairment, and that its beneficial effects are mediated, in part, via the enhancement of cholinergic signaling.
4. Nodakenin efficiently inhibits antigen-induced airway inflammation in asthmatic mouse, by reducing levels of IL-4,IL-5 and IL-13 in BALF,and IgE in serum,decreasing levels of nuclear P65 and p-P65 protein,increasing cytoplasmic P65 and IκBα protein,and NF-κB DNA binding activity.
5. Nodakenin can inhibit mast cell degranulation through the inhibition of IL-4 and TNF-α mRNA expression, and that nodakenin may potentially serve as an anti-allergic agent.
6. Nodakenin may be a potential therapeutic resource for AD as well as an adjunctive agent to control associated with AD, by suppressing the increase of AD-like skin lesions in ICR.
|Solvent:||Pyridine, Methanol, Ethanol, etc.|
|Storage:||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: firstname.lastname@example.org
|After receiving:||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.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||2.4486 mL||12.2429 mL||24.4858 mL||48.9716 mL||61.2145 mL|
|5 mM||0.4897 mL||2.4486 mL||4.8972 mL||9.7943 mL||12.2429 mL|
|10 mM||0.2449 mL||1.2243 mL||2.4486 mL||4.8972 mL||6.1214 mL|
|50 mM||0.049 mL||0.2449 mL||0.4897 mL||0.9794 mL||1.2243 mL|
|100 mM||0.0245 mL||0.1224 mL||0.2449 mL||0.4897 mL||0.6121 mL|
Biosci Biotechnol Biochem. 2014;78(9):1568-71.
|Effect of nodakenin on atopic dermatitis-like skin lesions.[Pubmed: 25209505]|
|Nodakenin is an important natural resource and medicinal material with anti-allergic and anti- inflammatory activities. We have previously shown that Nodakenin inhibits IgE/Ag-induced degranulation in mast cells. In this study, we investigated the inhibitory effect of Nodakenin on 2,4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis (AD)- like skin lesions in ICR mice. Scratching behavior, skin severity score, blood IgE level, and skin thickness were improved in DNCB-induced AD-like ICR mice. Our results showed that Nodakenin suppressed the increase of AD-like skin lesions in ICR mice. These results suggest that Nodakenin may be a potential therapeutic resource for AD as well as an adjunctive agent to control itching associated with AD.|
Immunopharmacol Immunotoxicol. 2014 Oct;36(5):341-8.
|The effects of nodakenin on airway inflammation, hyper-responsiveness and remodeling in a murine model of allergic asthma.[Pubmed: 25090633]|
|Compared with the model group, Nodakenin treatment markedly inhibited airway inflammation, hyper-responsiveness and remodeling, showing improvement in subepithelial fibrosis, smooth muscle hypertrophy, and goblet cell hyperplasia, and decreased levels of interleukin (IL)-4, IL-5, IL-13 and matrix metalloproteinase-2/-9 in bronchoalveolar lavage fluid, and the level of OVA-specific IgE in serum. In addition, the NF-κB DNA-binding activity in lung tissues was also reduced by Nodakenin treatment.|
J Pharmacol Exp Ther. 2012 Sep;342(3):654-64.
|Nodakenin suppresses lipopolysaccharide-induced inflammatory responses in macrophage cells by inhibiting tumor necrosis factor receptor-associated factor 6 and nuclear factor-κB pathways and protects mice from lethal endotoxin shock.[Pubmed: 22637723]|
|Nodakenin suppressed the transcriptional activity and translocation of nuclear factor-κB (NF-κB) by inhibiting inhibitory κB-α degradation and IκB kinase-α/β phosphorylation. In addition, Nodakenin was found to significantly inhibit the LPS-induced binding of transforming growth factor-β-activated kinase 1 to tumor necrosis factor receptor-associated factor 6 (TRAF6) by reducing TRAF6 ubiquitination. Pretreatment with Nodakenin reduced the serum levels of NO, PGE₂, and proinflammatory cytokines and increased the survival rate of mice with LPS-induced endotoxemia. Taken together, our data suggest that Nodakenin down-regulates the expression of the proinflammatory iNOS, COX-2, TNF-α, IL-6, and IL-1β genes in macrophages by interfering with the activation of TRAF6, thus preventing NF-κB activation.|
Life Sci. 2007 May 1;80(21):1944-50.
|Nodakenin, a coumarin compound, ameliorates scopolamine-induced memory disruption in mice.[Pubmed: 17382968 ]|
|Nodakenin is a coumarin compound initially isolated from the roots of Angelica gigas. In the present study, we investigated the effects of Nodakenin on learning and memory impairments induced by scopolamine (1 mg/kg, i.p.) using the passive avoidance test, the Y-maze test, and the Morris water maze test in mice. Nodakenin (10 mg/kg, p.o.) administration significantly reversed scopolamine-induced cognitive impairments in the passive avoidance test and the Y-maze test (P<0.05), and also reduced escape latency during training in the Morris water maze test (P<0.05). Moreover, swimming times and distances within the target zone of the Morris water maze were greater in the Nodakenin-treated group than in the scopolamine-treated group (P<0.05). In an in vitro study, Nodakenin was found to inhibit acetylcholinesterase activity in a dose-dependent manner (IC(50)=84.7 microM). In addition, Nodakenin was also found to inhibit acetylcholinesterase activity for 6 h in an ex-vivo study. These results suggest that Nodakenin may be a useful for the treatment of cognitive impairment, and that its beneficial effects are mediated, in part, via the enhancement of cholinergic signaling.|
Journal of Life Science,2011,21(12):1721-5.
|Anti-Allergic Effects of Nodakenin in IgE/Ag-Induced Type I Hypersensitivity.[Reference: WebLink]|
|Mast cells are major effector cells associated with allergic responses. They are activated through the release of histamine, arachidonic acid, and proinflammatory cytokines. We investigated the effect of Nodakenin, derived from the roots of Angelica gigas Nakai, on mast cell degranulation and on an allergic response in an animal model. We also investigated the effect of Nodakenin on expression of multiple cytokines. Nodakenin suppressed the release of β-hexosaminidase, a marker of degranulation, as well as the expression of interleukin IL-4 and TNF-α mRNA. Nodakenin inhibited the passive cutaneous anaphylaxis (PCA) reaction in ICR mice in a dose-dependent manner. These results suggest that Nodakenin can inhibit mast cell degranulation through the inhibition of IL-4 and TNF-α mRNA expression, and that Nodakenin may potentially serve as an anti-allergic agent.|
Basic & Clinical Medicine, 2014 , 34 (5) :690-4.
|Inhibitory effects of nodakenin on the airway inflammation and NF-κB signaling pathway in a murine asthmatic model.[Reference: WebLink]|
|To observe the effects of Nodakenin on airway inflammation in a mouse model of allergic asthma. Methods BALB / c mice were assigned randomly to one of the following four experimental groups: control, model,Nodakenin and dexamethasone. All test mice were sensitized and challenged by OVA to induce airway inflammation. One hour before OVA challenge,Nodakenin group was intragastrically administered with Nodakenin at a dose of 10 mg / kg,and dexamethasone group was intraperitoneally injected with dexamethasone a dose of 1 mg / kg. Airway responsiveness was measured by a lung function analysis systems. The number of total leukocytes in BALF was counted using a hemocytometer,and differential cells were counted using Diff-Quick-stained smears. Histopathology of lung tissue was analyzed by Hematoxylin-eosin staining. Levels of inflammatory mediators in serum or BALFs were measured by ELISA. The activity and expression of proteins in NF-κB signaling pathway was respectively evaluated by EMSA and western blot analysis. Results Compared with control group,the model groupexhibited obvious airway inflammation,airway reactivity was significantly increased,the level of total cells and differential cells was significantly increased,levels of IL-4,IL-5,IL-13,IgE were significantly increased,levels of nuclear P65 and p-P65 protein was significantly enhanced,level of cytoplasmic P65 and IκBα protein was significantly decreased,and the NF-κB DNA binding activity was significantly increased. Compared with model group, Nodakenin significantly suppressed airway inflammation,airway hyperreactivity,reduced levels of IL-4,IL-5 and IL-13 in BALF,and IgE in serum,decreased levels of nuclear P65 and p-P65 protein,increased cytoplasmic P65 and IκBα protein,and increased the NF-κB DNA binding activity. Conclusions Nodakenin efficiently inhibits antigen-induced airway inflammation in asthmatic mouse.|