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Dihydroquercetin (DHQ) ameliorated concanavalin A-induced mouse experimental fulminant hepatitis and enhanced HO-1 expression through MAPK/Nrf2 antioxidant pathway in RAW cells 期刊论文

编号：

26502ab6-c938-4f88-85d5-7123c05bb0e1
作者：

Zhao, Mingyi^[1,2];Chen, Jiajie(陈佳婕)^[1,3]Zhu, Ping^[1,4];Fujino, Masayuki^[1,5];Takahara, Terumi^[6];Toyama, Sumika^[1];Tomita, Amy^[1,7];Zhao, Lingling^[2];Yang, Zuocheng^[2];Hei, Mingyan^[2];Zhong, Liang(钟良)*Zhuang, Jian^[3,4];Kimura, Shuichi^[7];Li, XiaoKang^[1];
语种：

English
期刊：

INTERNATIONAL IMMUNOPHARMACOLOGY ISSN：1567-5769 2015 年 28 卷 2 期 (938 - 944) ; OCT
收录：
关键词：

Antioxidant ConA DHQ Hepatitis Mitogen-activated protein kinases HO-1 Nrf2
摘要：

Autoimmune hepatitis represents a ubiquitous human health problem and has a poor prognosis. Dihydroquercetin (DHQ), a well-known antioxidant, significantly inhibits fulminant hepatitis through antioxidant and anti-inflammation mechanisms. In this study, we show that administration of DHQ ameliorated concanavalin A (ConA)-induced mouse liver injury by increasing the survival rate, reducing the serum ALT and AST level, preventing histopathological injuries and decreasing pro-inflammatory cytokine mRNA expression in hepatic tissue. As macrophages/Kupffer cells in oxidative stress and pro-inflammatory mediators play an important role in the pathogenesis of immune-mediated hepatitis, we further exposed mouse RAW264 macrophage cell lines to ConA in vitro and found that DHQ significantly inhibited mRNA expression and secretion of IFN-gamma and TNF-alpha in cell culture supernatant. In addition, DHQ significantly enhanced heme oxygenase-1 (HO-1) expression in a dose-and time-dependent manner via increased Nrf2 expression in cytoplasm and nuclear translocation. Furthermore, DHQ enhanced phosphorylation of three members of the mitogen-activated protein kinase (MAPK) family, and cell treatment with MEK/ERK (PD98059), p38 (SE203580) and JNK (SP600125) inhibitors reduced DHQ-induced HO-1 expression. These results indicate that DHQ possesses hepatoprotective properties against ConA-induced liver injury, which are attributed to its ability to scavenge oxidative stress and to inhibit the release of inflammatory mediators via upregulation of HO-1 activity through the MAPK/Nrf2 signaling pathway in macrophages/Kupffer cells. (C) 2015 Elsevier B.V. All rights reserved.
推荐引用方式
GB/T 7714：

Zhao Mingyi,Chen Jiajie,Zhu Ping, et al. Dihydroquercetin (DHQ) ameliorated concanavalin A-induced mouse experimental fulminant hepatitis and enhanced HO-1 expression through MAPK/Nrf2 antioxidant pathway in RAW cells [J].INTERNATIONAL IMMUNOPHARMACOLOGY,2015,28(2):938-944.
APA：

Zhao Mingyi,Chen Jiajie,Zhu Ping,Fujino Masayuki,&Li Xiao-Kang.(2015).Dihydroquercetin (DHQ) ameliorated concanavalin A-induced mouse experimental fulminant hepatitis and enhanced HO-1 expression through MAPK/Nrf2 antioxidant pathway in RAW cells .INTERNATIONAL IMMUNOPHARMACOLOGY,28(2):938-944.
MLA：

Zhao Mingyi, et al. "Dihydroquercetin (DHQ) ameliorated concanavalin A-induced mouse experimental fulminant hepatitis and enhanced HO-1 expression through MAPK/Nrf2 antioxidant pathway in RAW cells" .INTERNATIONAL IMMUNOPHARMACOLOGY 28,2(2015):938-944.

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