Disease relevance of C10018

• In this model, a systemic administration of amentoflavone (30 mg/kg) markedly reduced the H-I-induced brain tissue loss with a wide therapeutic time window up to 6 h after the onset of hypoxia [1].
• Here, we report that amentoflavone significantly reduced cell death induced by staurosporine, etoposide and sodium nitroprusside in neuroblastoma SH-SY5Y cells [1].
• From the biflavonoids in SJW, only amentoflavone decreased SIH-induced hyperthermia in a dosage of 0.1 mg/kg [2].
• Hence amentoflavone, a dietary constituent, may be of therapeutic value for several lung diseases where COX-2 plays an important role [3].
• Among the nine biflavonoids tested, amentoflavone, ginkgetin, and isoginkgetin exhibited strong neuroprotection against cytotoxic insults induced by oxidative stress and amyloid beta, suggesting their therapeutic potential against neurodegenerative diseases, including ischemic stroke and Alzheimer's disease [4].

High impact information on C10018

• Amentoflavone blocked the activation of caspase 3, characteristic of apoptosis, and the proteolytic cleavage of its substrates following H-I injury [1].
• Furthermore, amentoflavone decreased the inflammatory activation of microglia after H-I injury when assessed by the microglial-specific marker OX-42 [1].
• Treatment of mouse microglial cells with amentoflavone resulted in a significant decrease in the lipopolysaccharide-induced production of nitric oxide and induction of inducible nitric oxide synthase and cyclo-oxygenase-2 [1].
• Amentoflavone, unlike apigenin, induced a static quenching effect, which denoted an important, but reversible, association of the molecule with the plasma membrane [5].
• Interactions of the monomeric and dimeric flavones apigenin and amentoflavone with the plasma membrane of L929 cells; a fluorescence study [5].

Chemical compound and disease context of C10018

• Downregulation of COX-2 and iNOS by amentoflavone and quercetin in A549 human lung adenocarcinoma cell line [6].

Biological context of C10018

• Vasorelaxation by amentoflavone isolated from Selaginella tamariscina [7].
• The IC50 of amentoflavone for CYP2C9 was 0.019 microg mL(-1) (0.035 microM) [8].
• Considering structure-activity relationship, methoxyl groups at 4' and 4''' in the B rings in amentoflavone-type biflavonoid might be important in osteoblast differentiation [9].
• NF-kappaB activation is controlled by the phosphorylation and subsequent degradation of I-kappaBalpha, and the cytosolic degradation of I-kappaBalpha was found to be inhibited by amentoflavone [10].
• Amentoflavone potently suppressed the reporter gene activity [10].

Anatomical context of C10018

• Transport of amentoflavone across the blood-brain barrier in vitro [11].
• These results suggest that amentoflavone relaxes vascular smooth muscle via endothelium-dependent nitric oxide-cGMP signaling, with possible involvement of non-specific K (+) and Ca (2+) channels [7].
• Amentoflavone induced concentration-dependent relaxation of the phenylephrine-precontracted aorta, which disappeared by removal of functional endothelium [7].
• Isolation of amentoflavone from Selaginella rupestris and its pharmacological activity on central nervous system, smooth muscles and isolated frog heart preparations [12].
• Using two electrode voltage-clamp methodology, amentoflavone has been shown to be a negative modulator of GABA at GABA(A) alpha(1)beta(2)gamma(2L) receptors expressed in Xenopus laevis oocytes This action appears to be independent of the flumazenil-sensitive benzodiazepine modulatory sites on the GABA(A) receptor [13].

Associations of C10018 with other chemical compounds

• Amentoflavone hexaacetate (AmAc) was synthesized from natural amentoflavone (Am), a biflavonoid extracted from Viburnum lantana L [14].
• The 74 samples of six HYPERICUM species (H. PERFOROTUM, H. HIRSUTUM, H. MACULATUM, H. TETRAPTERUM, H. MONTANUM, AND H. HUMIFUSUM) were collected around Slovenia and analysed for the content of ten substances (rutin, hyperoside, isoquercetin, quercitrin, quercetin, I3,II8-biapigenin, amentoflavone, pseudohypericin, hypericin, and hyperforin) [15].
• Levels of nine constituents (chlorogenic acid, rutin, hyperoside, isoquercitrin, quercitrin, quercetin, amentoflavone, pseudohypericin, and hypericin) were measured using liquid chromatography with ultraviolet/visible absorbance, mass spectrometric, and fluorescence detection [16].
• Chemical investigation on the constituents of the cones of Cycas beddomei has resulted in the isolation of a new biflavonoid, 2,3-dihydro-4'''-O-methyl amentoflavone, along with 2,3,2'',3''-tetrahydro hinokiflavone, 2,3,2'',3''-tetrahydro amentoflavone, 2,3-dihydro amentoflavone [17].
• In contrast, amentoflavone revealed an IC50 = 14.9 +/- 1.9 nM on benzodiazepine binding in vitro [18].

Gene context of C10018

• Treatment of 32D cells overexpressing the insulin receptor (IR) with amentoflavone resulted in a dose-dependent increase in tyrosine phosphorylation of IR [19].
• Inhibition of TNFalpha-induced cyclooxygenase-2 expression by amentoflavone through suppression of NF-kappaB activation in A549 cells [3].
• In contrast, amentoflavone although exerted no inhibitory effect on iNOS mRNA expression, did inhibit weakly iNOS protein expression [6].
• The LPS-induced activation of NF-kappaB was also found to be significantly blocked by amentoflavone, but AP-1 activation was unaffected [10].
• Bioassay-guided fractionation of MeOH extract of Selaginella tamariscina (Selaginellaceae) afforded a PTP1B inhibitory compound, amentoflavone [19].

Analytical, diagnostic and therapeutic context of C10018

• Quantification of amentoflavone was carried out by reversed phase HPLC in methanolic and aqueous extracts of the roots, stems and leaves [20].

References