Disease relevance of Superfustel K

• The objective of the current study was to examine the effect of fisetin on the cell cycle progression of the human colon cancer cell line HT-29 [1].
• The phosphorylation state of the retinoblastoma proteins shifted from hyperphosphorylated to hypophosphorylated in cells treated with 40 micromol/L fisetin [1].
• Hydroxylations and methylations of quercetin, fisetin, and catechin by Streptomyces griseus [2].
• We examined the effects of flavone and two polyhydroxylated plant flavonoids (quercetin and fisetin), either singly or in combination with ascorbic acid, on the growth of a human squamous cell carcinoma cell line (HTB 43) in vitro [3].
• Wogonin and fisetin induction of apoptosis through activation of caspase 3 cascade and alternative expression of p21 protein in hepatocellular carcinoma cells SK-HEP-1 [4].

Psychiatry related information on Superfustel K

• Together, these data demonstrate that the natural product fisetin can facilitate long-term memory, and therefore it may be useful for treating patients with memory disorders [5].

High impact information on Superfustel K

• Flavonoid fisetin promotes ERK-dependent long-term potentiation and enhances memory [5].
• Here we show that the flavonoid fisetin activates ERK and induces cAMP response element-binding protein (CREB) phosphorylation in rat hippocampal slices, facilitates long-term potentiation in rat hippocampal slices, and enhances object recognition in mice [5].
• A comparative study is presented of competitive fluorescences of three flavonols, 3-hydroxyflavone, 3,3',4',7-tetrahydroxyflavone (fisetin), and 4'-diethylamino-3-hydroxyflavone (DHF) [6].
• Quercetin or fisetin (a structural analog) inhibited the O-methylation of 2- and 4-hydroxyestradiol by a competitive plus noncompetitive mechanism (IC50 approximately 2-5 microM) [7].
• We found that each of the tea polyphenols [catechin, epicatechin, and (-)-epigallocatechin-3-O-gallate (EGCG)] and bioflavonoids (quercetin, fisetin, and myricetin) inhibited SssI DNMT- and DNMT1-mediated DNA methylation in a concentration-dependent manner [8].

Biological context of Superfustel K

• Wogonin and fisetin induce apoptosis in human promyeloleukemic cells, accompanied by a decrease of reactive oxygen species, and activation of caspase 3 and Ca(2+)-dependent endonuclease [9].
• Fisetin dose dependently inhibited both cell growth and DNA synthesis (P < 0.05), with a 79 +/- 1% decrease in cell number observed 72 h after the addition of 60 micromol/L fisetin [1].
• In addition, significant increases in the number of mis-segregating chromosomes were observed in fisetin-treated cells from both cell lines [10].
• The cells were treated with various concentrations of fisetin, and then were assessed for cell growth, QR activity, QR mRNA expression and transcription activation of the QR gene [11].
• Furthermore, transfection studies using a human QR antioxidant/electrophile-response element (ARE/EpRE) reporter construct demonstrated that fisetin activated the ARE/EpRE [11].

Anatomical context of Superfustel K

• In addition, fisetin inhibited IL-4 and IL-13 synthesis by anti-IgE antibody-stimulated human basophils (IC(50) = 5.1 and 6.2 micromol/L, respectively) and IL-4 synthesis by allergen-stimulated basophils from allergic patients (IC(50) = 4.8 micromol/L) [12].
• An increase in the pro-apoptotic protein, bax, and a decrease in the anti-apoptotic protein, Mcl-1, were detected in fisetin- and wogonin-treated HL-60 cells [9].
• HT-29 cells were cultured in serum-free medium with 0, 20, 40, or 60 micromol/L fisetin [1].
• Quercetin and fisetin, two naturally occurring bioflavonoids mobilized lipids and enzymes in the absence or presence of epinephrine in intact rat adipocytes [13].
• However, fisetin also inhibited CDk4 activity in a cell-free system (P < 0.05), indicating that it may directly inhibit CDk4 activity [1].

Associations of Superfustel K with other chemical compounds

• From these kinetic data we were able to calculate the redox potentials for dihydroquercetin, quercetin, rutin (a quercetin 3-glycoside), kaempferol, fisetin, and luteolin [14].
• RESULTS: Fisetin suppressed the induction of IL-4, IL-13, and IL-5 mRNA expression by A23187-stimulated KU812 cells and basophils in response to cross-linkage of the IgE receptor [12].
• In vitro chromatin digestion revealed that endonuclease activity was profoundly enhanced in wogonin- and fisetin-treated HL-60 cells, and the addition of ethylenediaminetetraacetic acid (EDTA) or ethyleneglycoltetraacetic acid (EGTA) into the reaction blocked endonuclease activation and at an optimum pH of 7 [9].
• In vitro, quercetin and its structural analog, fisetin, strongly inhibited the catechol-O-methyltransferase-catalyzed O-methylation of 60 microM 4-hydroxyestradiol, with IC50 values of approximately 2-4 microM [15].
• Conversely, myricetin and fisetin, which showed oxidation barely accelerated by the addition of BLM, inhibited DNA degradation promoted by ascorbate [16].

Gene context of Superfustel K

• Fisetin binds to the active form of CDK6, forming hydrogen bonds with the side chains of residues in the binding pocket that undergo large conformational changes during CDK activation by cyclin binding [17].
• The protein levels of cell division cycles (CDC)2 and CDC25C and the activity of CDC2 were also decreased in fisetin-treated cells (P < 0.05) [1].
• Fisetin decreased the activities of cyclin-dependent kinases (CDK)2 and CDK4; these effects were likely attributable to decreases in the levels of cyclin E and D1 and an increase in p21(CIP1/WAF1) levels (P < 0.05) [1].
• In human liver microsomes, troleandomycin inhibited C3'-OHP and C2-OHP formation, and a suitable inhibitor of human CYP2C8, fisetin, strongly inhibited the formation of 6 alpha-OHP, known to be catalyzed by human CYP2C8 [18].
• Fisetin inhibits the activities of cyclin-dependent kinases leading to cell cycle arrest in HT-29 human colon cancer cells [1].

Analytical, diagnostic and therapeutic context of Superfustel K

• However, renoprotection by fisetin was rapidly lost during rewarming [19].
• These results indicate that inhibition of cell cycle progression in HT-29 cells after treatment with fisetin can be explained, at least in part, by modification of CDK activities [1].
• These results show that fisetin increases QR activity by transcriptional activation of the ARE/EpRE, suggesting a novel mechanism by which dietary fisetin may be implicated in cancer chemoprevention [11].
• In this work, the interaction between fisetin (3,3',4',7-tetrahydroxyflavone) (Fis) and cyclodextrins (CDs) (alpha and beta) was studied through UV-vis absorption, steady-state fluorescence, induced circular dichroism, and (1)H NMR experiments with dependence on temperature and pH [20].
• Furthermore, flow cytometry analysis showed an increase of hypodiploid cells in wogonin- and fisetin-treated SK-HEP-1 cells [4].

References