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Int. J. Mol. Sci. 2014, 15(5), 8863-8877; doi:10.3390/ijms15058863

The Cytoprotective Effect of Sulfuretin against tert-Butyl Hydroperoxide-Induced Hepatotoxicity through Nrf2/ARE and JNK/ERK MAPK-Mediated Heme Oxygenase-1 Expression

1
Hanbang Body-Fluid Research Center, Wonkwang University, Iksan 570-749, Korea
2
College of Pharmacy, Wonkwang University, Iksan 570-749, Korea
3
Institute of Pharmaceutical Research and Development, College of Pharmacy, Wonkwang University, Iksan 570-749, Korea
4
Department of Pharmacy, Qingdao University of Science & Technology, Qingdao 266042, China
5
College of Pharmacy, Keimyung University, Dae-gu 704-701, Korea
6
Department of Biochemistry, Inha University School of Medicine, Incheon 400-712, Korea
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Received: 26 March 2014 / Revised: 12 May 2014 / Accepted: 13 May 2014 / Published: 19 May 2014
(This article belongs to the Section Biochemistry, Molecular and Cellular Biology)
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Abstract

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. View Full-Text
Keywords: sulfuretin; Rhus verniciflua Stokes; HepG2 cells; hepatoprotective; tert-butyl hydroperoxide; oxidative stress; heme oxygenase-1 sulfuretin; Rhus verniciflua Stokes; HepG2 cells; hepatoprotective; tert-butyl hydroperoxide; oxidative stress; heme oxygenase-1
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MDPI and ACS Style

Lee, D.-S.; Kim, K.-S.; Ko, W.; Li, B.; Jeong, G.-S.; Jang, J.-H.; Oh, H.; Kim, Y.-C. The Cytoprotective Effect of Sulfuretin against tert-Butyl Hydroperoxide-Induced Hepatotoxicity through Nrf2/ARE and JNK/ERK MAPK-Mediated Heme Oxygenase-1 Expression. Int. J. Mol. Sci. 2014, 15, 8863-8877.

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