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2014 ; 15
(5
): 8863-77
Nephropedia Template TP
gab.com Text
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English Wikipedia
The cytoprotective effect of sulfuretin against tert-butyl hydroperoxide-induced
hepatotoxicity through Nrf2/ARE and JNK/ERK MAPK-mediated heme oxygenase-1
expression
#MMPMID24857917
Lee DS
; Kim KS
; Ko W
; Li B
; Jeong GS
; Jang JH
; Oh H
; Kim YC
Int J Mol Sci
2014[May]; 15
(5
): 8863-77
PMID24857917
show ga
Sulfuretin is one of the major flavonoid components in Rhus verniciflua Stokes
(Anacardiaceae) isolates. In this study, we investigated the protective effects
of sulfuretin against tert-butyl hydroperoxide (t-BHP)-induced oxidative injury.
The results indicated that the addition of sulfuretin before t-BHP treatment
significantly inhibited cytotoxicity and reactive oxygen species (ROS) production
in human liver-derived HepG2 cells. Sulfuretin up-regulated the activity of the
antioxidant enzyme heme oxygenase (HO)-1 via nuclear factor E2-related factor 2
(Nrf2) translocation into the nucleus and increased the promoter activity of the
antioxidant response element (ARE). Moreover, sulfuretin exposure enhanced the
phosphorylation of c-Jun N-terminal kinase (JNK) and extracellular
signal-regulated kinase 1/2 (ERK1/2), which are members of the mitogen-activated
protein kinase (MAPK) family. Furthermore, cell treatment with a JNK inhibitor
(SP600125) and ERK inhibitor (PD98059) reduced sulfuretin-induced HO-1 expression
and decreased its protective effects. Taken together, these results suggest that
the protective effect of sulfuretin against t-BHP-induced oxidative damage in
human liver-derived HepG2 cells is attributable to its ability to scavenge ROS
and up-regulate the activity of HO-1 through the Nrf2/ARE and JNK/ERK signaling
pathways. Therefore, sulfuretin could be advantageous as a bioactive source for
the prevention of oxidative injury.