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Statements

Subject Item
n2:RIV%2F61989592%3A15310%2F13%3A33147793%21RIV14-GA0-15310___
rdf:type
skos:Concept n5:Vysledek
rdfs:seeAlso
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0074917
dcterms:description
Khellin and visnagin are two furanochromones that can be frequently found in ethnomedical formulations in Asia and the Middle East. Both compounds possess anti-inflammatory and analgesic properties, therefore modern medicine uses these compounds or structurally related derivatives for treatment of vitiligo, bronchial asthma and renal colics. Despite their frequent usage, the potential toxic properties of visnagin and khellin are not well characterized up-to-now. Many natural compounds modulate the expression and activity of cytochrome P450 1A1 (CYP1A1), which is well-known to bioactivate pro-carcinogens. The expression of this enzyme is controlled by the aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor and regulator of drug metabolism. Here, we investigated the influence of both furanochromones on AHR signaling in human HepG2 hepatocarcinoma cells and primary human hepatocytes. Both compounds transactivated xenobiotic response element (XRE)-driven reporter gene activity in a dose-dependent manner and induced CYP1A1 transcription in HepG2 cells and primary hepatocytes. The latter was abolished in presence of a specific AHR antagonist. CYP1A enzyme activity assays done in HepG2 cells and primary hepatocytes revealed an inhibition of enzyme activity by both furanochromones, which may become relevant regarding the metabolism of xenobiotics and co-administered therapeutic drugs. The observed induction of several other members of the AHR gene battery, whose gene products are involved in regulation of cell growth, differentiation and migration, indicates that a further toxicological characterization of visnagin and khelllin is urgently required in order to minimize potential drug-drug interactions and other toxic side-effects that may occur during therapeutic usage of these furanochromones. Khellin and visnagin are two furanochromones that can be frequently found in ethnomedical formulations in Asia and the Middle East. Both compounds possess anti-inflammatory and analgesic properties, therefore modern medicine uses these compounds or structurally related derivatives for treatment of vitiligo, bronchial asthma and renal colics. Despite their frequent usage, the potential toxic properties of visnagin and khellin are not well characterized up-to-now. Many natural compounds modulate the expression and activity of cytochrome P450 1A1 (CYP1A1), which is well-known to bioactivate pro-carcinogens. The expression of this enzyme is controlled by the aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor and regulator of drug metabolism. Here, we investigated the influence of both furanochromones on AHR signaling in human HepG2 hepatocarcinoma cells and primary human hepatocytes. Both compounds transactivated xenobiotic response element (XRE)-driven reporter gene activity in a dose-dependent manner and induced CYP1A1 transcription in HepG2 cells and primary hepatocytes. The latter was abolished in presence of a specific AHR antagonist. CYP1A enzyme activity assays done in HepG2 cells and primary hepatocytes revealed an inhibition of enzyme activity by both furanochromones, which may become relevant regarding the metabolism of xenobiotics and co-administered therapeutic drugs. The observed induction of several other members of the AHR gene battery, whose gene products are involved in regulation of cell growth, differentiation and migration, indicates that a further toxicological characterization of visnagin and khelllin is urgently required in order to minimize potential drug-drug interactions and other toxic side-effects that may occur during therapeutic usage of these furanochromones.
dcterms:title
Khellin and visnagin differentially modulate AHR signaling and downstream CYP1A activity in human liver cells Khellin and visnagin differentially modulate AHR signaling and downstream CYP1A activity in human liver cells
skos:prefLabel
Khellin and visnagin differentially modulate AHR signaling and downstream CYP1A activity in human liver cells Khellin and visnagin differentially modulate AHR signaling and downstream CYP1A activity in human liver cells
skos:notation
RIV/61989592:15310/13:33147793!RIV14-GA0-15310___
n5:predkladatel
n6:orjk%3A15310
n3:aktivita
n16:S n16:P
n3:aktivity
P(GAP303/12/0472), P(GBP303/12/G163), S
n3:cisloPeriodika
9
n3:dodaniDat
n11:2014
n3:domaciTvurceVysledku
n17:4908171 n17:8069239
n3:druhVysledku
n20:J
n3:duvernostUdaju
n15:S
n3:entitaPredkladatele
n8:predkladatel
n3:idSjednocenehoVysledku
82620
n3:idVysledku
RIV/61989592:15310/13:33147793
n3:jazykVysledku
n19:eng
n3:klicovaSlova
dioxin; repressor; SRC kinase; mice lacking; MCF10A cells; human hepatocytes; cytochrome-P450 1A1; transcriptional regulation; arylhydrocarbon receptor
n3:klicoveSlovo
n10:SRC%20kinase n10:repressor n10:MCF10A%20cells n10:mice%20lacking n10:dioxin n10:human%20hepatocytes n10:transcriptional%20regulation n10:cytochrome-P450%201A1 n10:arylhydrocarbon%20receptor
n3:kodStatuVydavatele
US - Spojené státy americké
n3:kontrolniKodProRIV
[7E63027A8460]
n3:nazevZdroje
PLoS One
n3:obor
n21:FR
n3:pocetDomacichTvurcuVysledku
2
n3:pocetTvurcuVysledku
6
n3:projekt
n13:GBP303%2F12%2FG163 n13:GAP303%2F12%2F0472
n3:rokUplatneniVysledku
n11:2013
n3:svazekPeriodika
8
n3:tvurceVysledku
Abel, Josef Dvořák, Zdeněk Proksch, Peter Haarmann-Stemmann, Thomas Vrzal, Radim Frauenstein, Katrin
n3:wos
000324777300054
s:issn
1932-6203
s:numberOfPages
10
n7:doi
10.1371/journal.pone.0074917
n9:organizacniJednotka
15310