Disease relevance of quercitrin

• When tested in chronic colitis (2 and 4 weeks), quercitrin treatment (1 or 5 mg/kg.day) decreased colonic damage score and the incidence of diarrhea, and normalized the colonic fluid transport [1].
• Quercitrin-treated rats had less diarrhoeal output and did not show mucosal hyperplasia after three days of treatment [2].
• The flavonoids hyperoside, isoquercitrin and quercitrin (all at 0.6 mg/kg, P. O.) and rutin (1 mg/kg, P. O.) only partially blocked OF-induced hyperthermia [3].
• In the present study, we investigated the protective mechanism of quercetin (QUE) and its glycosides, rutin (RUT) and quercitrin (QUI), on reactive oxygen species (ROS)-dependent (H(2)O(2)) and -independent (chemical anoxia) cell death in rat glioma C6 cells [4].
• The combined application of quercitrin and 5-ethyl-2'-deoxyuridine showed a synergic effect on pseudorabies virus [5].

High impact information on quercitrin

• Quercetin, quercitrin, and myricitrin are significantly more potent than the previously known aldose reductase inhibitors [6].
• The unactivated enzyme was strongly inhibited by aldose reductase inhibitors such as sorbinil, alrestatin, and quercetrin, and by phosphorylated intermediates such as ADP, glycerate 3-phosphate, glycerate 1,3-bisphosphate, and glycerate 2,3-trisphosphate [7].
• However, such results have not been reproduced in in vivo experimental models of intestinal inflammation, in which quercetin did not show beneficial effects while its glycosides, quercitrin or rutin, have demonstrated their effectiveness [8].
• Previous in vitro experiments have shown that quercetin exerts a bigger effect than quercitrin in the down-regulation of the inflammatory response [8].
• Of the drugs examined (genistein, quercetin, quercitrin, etoposide, m-AMSA, CP-115,953, and novobiocin), only novobiocin was unable to enhance topoisomerase II-mediated DNA cleavage [9].

Chemical compound and disease context of quercitrin

• BACKGROUND AND AIMS: Previous studies have described the intestinal anti-inflammatory effects exerted by the bioflavonoid quercitrin (QR) and by an n-3 polyunsaturated fatty acids (PUFA)-enriched diet in experimental models of rat colitis [10].
• This study focuses on the effect of quercitrin (1 and 5 mg/kg) in the early stages (24 h) of trinitrobenzene sulfonic acid colitis [11].
• Quercetin and quercitrin reduced the yields of Human (alpha) herpesvirus 1 (HSV-1) and Suid (alpha) herpesvirus 1 (pseudorabies virus), but hesperidin and rutin had no effect [12].

Biological context of quercitrin

• Glycosidation with L-sugar (quercitrin and guaijaverin), however, improved the inhibitory activity (the IC50 values being 1 X 10(-6) M and 2.5 X 10(-6) M respectively) [13].
• Quercetin, but not rutin and quercitrin, prevention of H2O2-induced apoptosis via anti-oxidant activity and heme oxygenase 1 gene expression in macrophages [14].
• Quercitrin, a glycoside form of quercetin, prevents lipid peroxidation in vitro [15].
• Most of the enzymatic preparations showed broad substrate specificity, and some of them were also acting on sterically hindered substrates (e.g., quercitrin) [16].
• The presence of chenodeoxycholic or deoxycholic acids in the quercitrin-induced culture resulted in a fecal preparation which enhanced the mutagenesis of quercitrin approximately two-fold at optimal concentrations of 0.6 mM and 0.8 mM respectively [17].

Anatomical context of quercitrin

• Reductive metabolism of metyrapone by a quercitrin-sensitive ketone reductase in mouse liver cytosol [18].
• When quercitrin (1 mg kg(-1) day(-1)) was administered on established colitis, it facilitated the recovery of the inflamed mucosa [19].
• Down-regulatory effect of quercitrin gallate on nuclear factor-kappa B-dependent inducible nitric oxide synthase expression in lipopolysaccharide-stimulated macrophages RAW 264.7 [20].
• Immunohistochemical studies showed that quercitrin treatment reduced macrophage and granulocyte infiltration in the inflamed tissue [19].
• The acute anti-inflammatory effect of quercitrin is unrelated to impairment of neutrophil function or lipoxygenase inhibition, and it may be caused by mucosal protection or enhancement of mucosal repair secondary to increased defense against oxidative insult and/or preservation of normal colonic absorptive function [1].

Associations of quercitrin with other chemical compounds

• The enzyme involved was characterized as a NADPH-dependent carbonyl reductase which is strongly inhibited by the plant flavonoid quercitrin but which shows no sensitivity to phenobarbital [18].
• In conclusion, carbonyl reduction of metyrapone in continuous cell lines is mediated by carbonyl reductases due to the common sensitivity towards the diagnostic inhibitor quercitrin and due to the strong preference for NADPH as cosubstrate [21].
• The concentrations of hyperforin, hypericin, and quercitrin in the plant extracts were determined by HPLC, and an "artificial extract" containing the same mixture of these constituents was investigated [22].
• Further separation of fraction IIa by preparative HPLC yielded fraction IIa1 which mainly was composed of hyperoside, isoquercitrin, miquelianin and quercitrin, and fraction IIa2 which contained small amounts of hyperoside and astilbin, while most compounds were not known [23].
• 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) [24].

Gene context of quercitrin

• QUE, but not RUT or QUI, caused rapid and transient induction of caspase 3/CPP32 activity, but not caspase 1 activity, according to cleavage of caspase 3 substrates poly(ADP-ribose) polymerase (PARP) and D4-GDI proteins, and the appearance of cleaved caspase 3 fragments being detected in QUE- but not RUT- or QUI-treated HL-60 cells [25].
• Similarly, alrestatin and quercitrin also are potent inhibitors of aldehyde reductase I and aldehyde reductase II [26].
• The intestinal anti-inflammatory effect of quercitrin is associated with an inhibition in iNOS expression [19].
• The reaction was strongly inhibited by quercitrin, a specific inhibitor of carbonyl reductase [27].
• Isolation of quercetin-3-O-L-rhamnoside from Acer truncatum Bunge by high-speed counter-current chromatography [28].

Analytical, diagnostic and therapeutic context of quercitrin

• Selective extraction of quercetrin in vegetable drugs and urine by off-line coupling of boronic acid affinity chromatography and high-performance liquid chromatography [29].
• Oral administration of quercitrin modifies intestinal oxidative status in rats [30].

References