Aromadendrin CAS NO.480-20-6

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General tips：For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging：1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
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Chemical Properties of Aromadendrin

Source of Aromadendrin

1 Equisetum sp. 2 Ginkgo sp. 3 Larix sp. 4 Morus sp. 5 Origanum sp. 6 Pinus sp. 7 Salix sp. 8 Silybum sp. 9 Thuja sp. 10 Thymus sp.

Biological Activity of Aromadendrin

Preparing Stock Solutions of Aromadendrin

References on Aromadendrin

Aromadendrin Inhibits Lipopolysaccharide-Induced Nuclear Translocation of NF-kappaB and Phosphorylation of JNK in RAW 264.7 Macrophage Cells.[Pubmed:24265867]

Biomol Ther (Seoul). 2013 May 30;21(3):216-21.

Aromadendrin, a flavonol, has been reported to possess a variety of pharmacological activities such as anti-inflammatory, antioxidant, and anti-diabetic properties. However, the underlying mechanism by which Aromadendrin exerts its biological activity has not been extensively demonstrated. The objective of this study is to elucidate the anti-inflammatory mechanism of aromadedrin in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. Aromadendrin significantly suppressed LPS-induced excessive production of pro-inflammatory mediators such as nitric oxide (NO) and PGE2. In accordance, Aromadendrin attenuated LPSinduced overexpression iNOS and COX-2. In addition, Aromadendrin significantly suppressed LPS-induced degradation of IkappaB, which sequesters NF-kappaB in cytoplasm, consequently inhibiting the nuclear translocation of pro-inflammatory transcription factor NF- kappaB. To elucidate the underlying signaling mechanism of anti-inflammatory activity of Aromadendrin, MAPK signaling pathway was examined. Aromadendrin significantly attenuated LPS-induced activation of JNK, but not ERK and p38, in a concentration-dependent manner. Taken together, the present study clearly demonstrates that Aromadendrin exhibits anti-inflammatory activity through the suppression of nuclear translocation of NF-kappaB and phosphorylation of JNK in LPS-stimulated RAW 264.7 macrophage cells.

Stimulation of glucose uptake and improvement of insulin resistance by aromadendrin.[Pubmed:22056597]

Pharmacology. 2011;88(5-6):266-74.

Agents that stimulate glucose uptake and improve insulin resistance may be useful in the management of type 2 diabetes mellitus (DM). Thus, the aims of this study were to assess the effects of Aromadendrin, a flavonoid from Gleditsia sinensis Lam., on stimulation of glucose uptake and improvement of insulin resistance and to characterize the molecular mechanisms underlying these activities. Insulin-stimulated glucose uptake was measured in HepG2 cells and in differentiated 3T3-L1 adipocytes using 2-[N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino]-2-deoxy-D-glucose (2-NBDG), a fluorescent D-glucose analog. Expression of the peroxisome proliferator-activated receptor-gamma2 (PPARgamma2) and adipocyte-specific fatty acid binding protein (aP2) mRNAs and the PPARgamma2 protein was analyzed in adipocytes using RT-PCR and immunoblotting, respectively. Insulin-stimulated protein kinase B (Akt/PKB) phosphorylation was measured in high glucose-induced, insulin-resistant HepG2 cells. Similar to 30 mumol/l rosiglitazone, treatment with 30 mumol/l Aromadendrin significantly stimulated insulin-sensitive glucose uptake in both HepG2 cells and 3T3-L1 adipocytes. Aromadendrin treatment also enhanced adipogenesis and caused increases in the expression of PPARgamma2 and aP2 mRNAs and the PPARgamma2 protein in differentiated 3T3-L1 adipocytes. In high glucose-induced, insulin-resistant HepG2 cells, Aromadendrin reversed the inhibition of Akt/PKB phosphorylation in response to insulin, which could be abrogated by pretreatment with LY294002, a phosphatidylinositol 3-kinase (PI3K) inhibitor. Aromadendrin treatment induced adipogenesis by increases in PPARgamma2 expression, resulting in stimulation of glucose uptake and ameliorated insulin resistance. These findings suggest that Aromadendrin may represent a potential therapeutic candidate for the management of type 2 DM.

Description

Dihydrokaempferol is isolated from Bauhinia championii (Benth). Dihydrokaempferol induces apoptosis and inhibits Bcl-2 and Bcl-xL expression. Dihydrokaempferol is a good candidate for new antiarthritic drugs.

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