Disease relevance of Ephdine

• To investigate the mechanistic basis for the biological properties of anthocyanins, two aglycone anthocyanins [delphinidin (DY) and cyanidin (CY)] were used to examine their effects on cell cycle progression and on induction of apoptosis in human cancer cells (uterine carcinoma and colon adenocarcinoma cells) and in normal human fibroblasts [1].
• In this work, we report that the aglycons of the most abundant anthocyanins in fruits, cyanidin (Cy), delphinidin (Dp), and petunidin (Pt), act as potent inhibitors of glioblastoma cell migration [2].
• Inhibitory effect of delphinidin from Solanum melongena on human fibrosarcoma HT-1080 invasiveness in vitro [3].
• At 200 microg/mL, cyanidin, delphinidin and petunidin inhibited the breast cancer cell growth by 47, 66 and 53%, respectively [4].
• The purpose of the present study was to investigate the effects of the flavonoid delphinidin chloride (CAS 528-53-0, IdB 1056) on diabetic microangiopathy [5].

High impact information on Ephdine

• MS and NMR spectroscopy clarified that the chemical structure of the metabolite was 4'-O-methyl delphinidin 3-O-beta-d-glucopyranoside (methylation of the 4'-OH on the delphinidin B-ring) [6].
• Characterization of the enzymatic properties using the recombinant 3'GT protein revealed that, in contrast to most of flavonoid glucosyltransferases, it has strict substrate specificity: 3'GT specifically glucosylates the 3'-hydroxy group of delphinidin-type anthocyanins containing Glc groups at 3 and 5 positions [7].
• METHODS AND RESULTS: Vascular endothelial growth factor-stimulated human umbilical endothelial cell migration and proliferation are potently inhibited by delphinidin [8].
• Involvement of cyclin-dependent pathway in the inhibitory effect of delphinidin on angiogenesis [8].
• The purpose of this study was to define the effect of delphinidin, a vasoactive polyphenol belonging to the class of anthocyanin, on endothelial cell proliferation and migration as well as on in vivo angiogenesis [8].

Chemical compound and disease context of Ephdine

• Overall, these results demonstrate that Dp, Pt, and Cy affect plasminogen activation, thus leading to the inhibition of glioblastoma cell migration and therefore they may be helpful for the development of new strategies for cancer prevention and therapy [2].

Biological context of Ephdine

• Flow cytometric analysis demonstrates that delphinidin inhibition of proliferation is correlated with the blockade of cell cycle in G(0)/G(1) phase [8].
• Western blotting analysis indicated that delphinidin inhibited the degradation of IkappaB-alpha, nuclear translocation of p65 and CCAAT/enhancer-binding protein (C/EBP)delta and phosphorylation of c-Jun, but not CRE-binding protein (CREB) [9].
• 6. All of the observed effects of delphinidin may preserve endothelium integrity, the alteration of which lead to pathologies including cardiovascular diseases, such as atherosclerosis, and is often associated with cancers [10].
• Among the anthocyanins, delphinidin (maximal relaxation being 89%), but not malvidin or cyanidin, showed endothelium-dependent vasorelaxation [11].
• Delphinidin, an active compound of red wine, inhibits endothelial cell apoptosis via nitric oxide pathway and regulation of calcium homeostasis [10].

Anatomical context of Ephdine

• Furthermore, delphinidin inhibits neovascularisation in vivo in chorioallantoic membrane model [8].
• Delphinidin inhibited serum- and vascular endothelium growth factor-induced BAECs proliferation [12].
• Delphinidin and cyanidin inhibit PDGF(AB)-induced VEGF release in vascular smooth muscle cells by preventing activation of p38 MAPK and JNK [13].
• However, metabolites such as 4'-O-methyl analogues and extended glucuronides which were observed for delphinidin 3-O-beta-D-glucopyranoside and cyanidin 3-O-beta-D-glucopyranoside metabolisms were not detected in urine or blood plasma [14].
• Incubation of juices with the rat small intestine cell extracts at neutral pH appeared to decrease the levels of delphinidin glucosides more than the levels of cyanidin glucosides [15].

Associations of Ephdine with other chemical compounds

• In delphinidin producing petunia plants, the mRNAs corresponding to the eggplant P-450 and flavonoid biosynthesis genes such as CHS and DFR were most abundant during the mid stage of flower bud development, but could not be detected in leaf tissues [16].
• The tannins, delphinidin and procyanidin were isolated from flowers of white clover (Trifolium repens) and the leaves of Arnot Bristly Locust (Robina fertilis) respectively, and tested for mutagenic properties in a range of systems [17].
• The major phenolic antioxidant components of egg plant are chlorogenic acid in the flesh and a delphinidin conjugate in the skin [18].
• The relative floral anthocyanidin contents of 195 commercial petunias with floral colours other than white and yellow were determined using HPLC, and the presence of five anthocyanidins (cyanidin, peonidin, delphinidin, petunidin, and malvidin) was confirmed [19].
• Antioxidant activities of freeze-dried preparations of a 70% acetone extract of pomegranate (Punica granatum L.) and its three major anthocyanidins (delphinidin, cyanidin, and pelargonidin) were evaluated [20].

Gene context of Ephdine

• Delphinidin, the most potent inhibitor, caused a dose-dependent inhibition of COX-2 expression at both mRNA and protein levels [9].
• The aglycons of the most abundant anthocyanins in food, cyanidin (cy) and delphinidin (del), represent potent inhibitors of the epidermal growth factor receptor (EGFR) [21].
• 4. Western blot analysis and protein detection by confocal microscopy demonstrate that the antiapoptotic effect of delphinidin was associated with an increased endothelial NOS expression mediated by a MAP kinase pathway [10].
• Concomitant with the apoptosis, delphinidin stimulates JNK pathway activation including JNK phosphorylation and c-jun gene expression, and activates caspase-3 [22].
• According to the appearance of the caspase-3 fragments and stimulated proteolytic cleavage of poly (ADP-ribose) polymerase (PARP) in time-dependent studies, delphinidin induced apoptotic cell death characterized by internucleosomal DNA fragmentation and caused a rapid induction of caspase-3 activity [23].

Analytical, diagnostic and therapeutic context of Ephdine

• A delphinidin-based pigment in the crude extract from cell cultures was identical to the major flower pigment as shown by HPLC co-chromatography [24].
• High-performance liquid chromatography diode array detection-mass spectrometry analysis showed that delphinidin 3-O-rutinoside represented about 62.4% of the total pigments [25].
• Paper chromatography suggested delphinidol to be the only anthocyanidin detectable in the material obtained by acidic hydrolysis of the polymeric polyphenol fraction [26].
• By means of electrospray ionization mass spectrometry and one- and two-dimensional nuclear magnetic resonance spectroscopy, its structure was determined to be delphinidin 3-O-(2-O-beta-D-glucopyranosyl-alpha-l-arabinopyranoside) [27].
• Thus, the goal of this study was to evaluate both the antimutagenicity/antigenotoxicity and mutagenicity/genotoxicity of aqueous extract obtained from the Solanum melanogena, a possible novel source of anthocyanin, and its main purified anthocyanin extract (delphinidin), using the single cell (comet) assay and micronucleus test [28].

References