Aurantio-obtusin possesses anti-allergic, vasorelaxation, hypotensive and hypolipidemic effects, it is a promising osteoanabolic compound with potential therapeutic applications in the prevention of osteoporosis and other metabolic bone diseases. Aurantio-obtusin can inhibit allergic responses in IgE-mediated mast cells and anaphylactic models, it suppresses degranulation, histamine production, and reactive oxygen species generation and inhibits the production and mRNA expression of tumor necrosis factor-α and interleukin-4, and also suppresses the prostaglandin E2 production and expression of cyclooxygenase 2.
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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.
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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.
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J Agric Food Chem. 2015 Oct 21;63(41):9037-46.
Cassia tora Seed Extract and Its Active Compound Aurantio-obtusin Inhibit Allergic Responses in IgE-Mediated Mast Cells and Anaphylactic Models.[Pubmed: 26434611
Cassia tora seed is widely used due to its various biological properties including anticancer, antidiabetic, and anti-inflammatory effects. However, there has been no report of the effects of C. tora seed extract (CTE) on immunoglobulin E (IgE)-mediated allergic responses.
METHODS AND RESULTS:
In this research, we demonstrated the effects of CTE and its active compound Aurantio-obtusin on IgE-sensitized allergic reactions in mast cells and passive cutaneous anaphylaxis (PCA). CTE and Aurantio-obtusin suppressed degranulation, histamine production, and reactive oxygen species generation and inhibited the production and mRNA expression of tumor necrosis factor-α and interleukin-4. CTE and Aurantio-obtusin also suppressed the prostaglandin E2 production and expression of cyclooxygenase 2. Furthermore, CTE and Aurantio-obtusin suppressed IgE-mediated FcεRI signaling such as phosphorylation of Syk, protein kinase Cμ, phospholipase Cγ, and extracellular signal-regulated kinases. CTE and Aurantio-obtusin blocked mast cell-dependent PCA in IgE-mediated mice.
These results suggest that CTE and Aurantio-obtusin are a beneficial treatment for allergy-related diseases.
Planta Med. 2014 May;80(7):544-9.
Aurantio-obtusin stimulates chemotactic migration and differentiation of MC3T3-E1 osteoblast cells.[Pubmed: 24841966
Osteoporosis is one of the major metabolic bone diseases and is among the most challenging noncommunicable diseases to treat. Although there is an increasing interest in identifying bioactive molecules for the prevention and management of osteoporosis, such studies principally focus only on differentiation and mineralization of osteoblasts or inhibition of osteoclast activity. Stimulation of osteoblast migration must be a promising osteoanabolic strategy for improved metabolic bone disease therapy.
METHODS AND RESULTS:
In this study, we show that an anthraquinone derivative, Aurantio-obtusin, stimulated chemotactic migration of MC3T3-E1 osteoblast cells in a concentration-dependent manner. The use of a real-time chemotaxis analyzing system, TAXIScan, facilitated the evaluation of both velocity and directionality of osteoblast migration in response to the compound. Besides migration, the compound stimulated osteoblast differentiation and mineralization.
Taken together, the data presented in this paper demonstrate that Aurantio-obtusin is a promising osteoanabolic compound of natural origin with potential therapeutic applications in the prevention of osteoporosis and other metabolic bone diseases.
Journal of Analytical Science,2016, 32(2):178-82.
Metabolomics-based Study of the Lipid Regulating Effect of Aurantio-obtusin on Hyperlipidemia Rats.[Reference: WebLink
The influences of Aurantio-obtusin on endogenous metabolites in blood of hyperlipemia rats were investigated by metabonomics method in order to find the related biomarkers.
METHODS AND RESULTS:
The rat model was established by hyperlipidemia rats that were raised by high fat diet and then treated with intragastric administration of Aurantio-obtusin.Metabolites in plasma of hyperlipidemia rats were accurately analyzed by gas chromatography-mass spectrometry.In order to find out the potential biomarkers,principal component analysis,partial least squares discriminant analysis and random forest algorithm were used to study the changes of endogenous metabolite profiles in rats before modeling after modeling and after drug treatments.Ten potential biomarkers were obtained as the final achievement:alanine,glycine,valine,isoleucine,fumaric acid,serine,1,5-anhydro-D-ghlcitol,linoleic acid,stearic acid and cholesterol.
This investigation demonstrates that aurantio has a good lipid regulating effect mainly by affecting the body amino acid and fatty acid metabolism.
J Pharmacol Sci. 2015 Jul;128(3):108-15.
Aurantio-obtusin relaxes systemic arteries through endothelial PI3K/AKT/eNOS-dependent signaling pathway in rats.[Pubmed: 26076958
Aurantio-obtusin is a natural effective compound isolated from Semen Cassiae, which possesses hypotensive and hypolipidemic effects. Although its hypotensive effect have been clarified, mechanisms Aurantio-obtusin relaxes systemic arteries remain unclear. This study was to investigate effects and mechanisms of Aurantio-obtusin on isolated mesenteric arteries (MAs).
METHODS AND RESULTS:
We examined MAs relaxation induced by Aurantio-obtusin on rat isolated MAs, expression and activity of endothelial nitric oxide synthase (eNOS) and protein kinase B (AKT), and nitric oxide (NO) production in bovine artery endothelial cells (BAECs). Findings showed Aurantio-obtusin elicited dose-dependent vasorelaxation with phenylephrine (PE) precontracted rat MA rings (diameter: 200-300 μm), which can be diminished by denudation of endothelium and inhibition of eNOS activity, while having no effect on rat isolated pulmonary artery (PA) rings. Aurantio-obtusin increased NO production by promoting phosphorylations of eNOS at Ser-1177 and Thr-495 in endothelial cells. Aurantio-obtusin also promoted phosphorylations of Akt at Ser-473. PI3K inhibitor LY290042 could diminish vasorelaxation induced by Aurantio-obtusin. Moreover Aurantio-obtusin also elicited dose-dependent vasorelaxation effect with PE precontracted MA rings (diameter: 100-150 μm). Therefore, vasorelaxation induced by Aurantio-obtusin was dependent on endothelium integrity and NO production, which mediated by endothelial PI3K/Akt/eNOS pathway.
Results suggest Aurantio-obtusin may offer therapeutic effects in hypertension, as a new potential vasodilator.
Phytother Res. 2014 Oct;28(10):1577-80.
Biotransformation of glucoaurantio-obtusin towards aurantio-obtusin increases the toxicity of irinotecan through increased inhibition towards SN-38 glucuronidation.[Pubmed: 24842785
The present study aims to investigate the influence of irinotecan's toxicity by the biotransformation of glucoAurantio-obtusin to Aurantio-obtusin.
METHODS AND RESULTS:
Intraperitoneal administration (i.p.) of 100 mg/kg Aurantio-obtusin significantly increased the toxicity of irinotecan, but the i.p. administration of 100 mg/kg glucoAurantio-obtusin showed negligible influence towards irinotecan's toxicity. Furthermore, the mechanism was explained through determining the inhibition potential of glucoAurantio-obtusin and Aurantio-obtusin towards the glucuronidation metabolism of SN-38 that has been regarded to be the major active product responsible for the toxicity of irinotecan. The results showed that Aurantio-obtusin exhibited strong competitive inhibition towards the glucuronidation of SN-38, but negligible inhibition potential of glucoAurantio-obtusin towards SN-38 glucuronidation was observed.
These results showed that biotransformation of glucoAurantio-obtusin towards Aurantio-obtusin increased the toxicity of irinotecan through increased inhibition of SN-38 glucuronidation.