Aromadendrin

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

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

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.
METHODS AND RESULTS:
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-γ2 (PPARγ2) and adipocyte-specific fatty acid binding protein (aP2) mRNAs and the PPARγ2 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 μmol/l rosiglitazone, treatment with 30 μmol/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 PPARγ2 and aP2 mRNAs and the PPARγ2 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 PPARγ2 expression, resulting in stimulation of glucose uptake and ameliorated insulin resistance.
CONCLUSIONS:
These findings suggest that Aromadendrin may represent a potential therapeutic candidate for the management of type 2 DM.

Food Sci. Biotechnol., 2011, 20(5):1283-8.

Inhibitory Activity of Aromadendrin from Prickly Pear (Opuntia ficus-indica) Root on Aldose Reductase and the Formation of Advanced Glycation End Products.[Reference: WebLink]

Prickly pear (Opuntia ficus-indica) is a longdomesticated crop plant of arid and semiarid parts of the world.
METHODS AND RESULTS:
The efficacy of extracts of prickly pear root for managing diabetes and diabetes complications was evaluated using a variety of in vitro bioassays. The ethyl acetate-soluble fraction was most effective in the prevention of diabetes and its complications via the inhibition of rat lens aldose reductase activity, the formation of advanced glycation end products, and α-glucosidase activity.
CONCLUSIONS:
MS and NMR were used to identify the bioactive compound from the ethyl acetate-soluble fraction as 3,5,7,4′-tetrahydroxyflavanone (Aromadendrin).

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

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

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.
METHODS AND RESULTS:
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 IκB, which sequesters NF-κB in cytoplasm, consequently inhibiting the nuclear translocation of pro-inflammatory transcription factor NF- κB. 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.
CONCLUSIONS:
Taken together, the present study clearly demonstrates that Aromadendrin exhibits anti-inflammatory activity through the suppression of nuclear translocation of NF-κB and phosphorylation of JNK in LPS-stimulated RAW 264.7 macrophage cells.