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Protective effect of SKLB010 against D-galactosamine/lipopolysaccharide-induced acute liver failure via nuclear factor-κB signaling pathway in macrophages.

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机构： [1]State Key Laboratory of Biotherapy,West China Hospital, West China Medical School, Sichuan University, Chengdu, China [2]Institute of Burn Research, Southwest Hospital, State Key laboratory of Trauma, Burns & Combined Injury, Third Military Medical University, Chongqing, China [3]The First People's Hospital of Ji'an City, Jiangxi, China

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关键词： Acute liver failure SKLB010 LPS Macrophage NF-κB

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Acute liver failure is characterized by the sudden loss of hepatic function and a high mortality. SKLB010, a derivative of thiazolidinediones, has been proved to be effective in protecting mice from acute liver failure caused by concanavalin A and carbon tetrachloride in our previous work. The purpose of the current study was to evaluate whether SKLB010 could prevent acute liver injury caused by d-galactosamine/lipopolysaccharide (LPS) in mice, and to investigate the underlying mechanisms. In the macrophage-mediated D-GalN/LPS model of acute liver injury, serum enzyme activity was suppressed and liver injury was attenuated by SKLB010. The serum levels of TNF-α and hepatic TNF-α mRNA expression were also markedly decreased after the treatment of SKLB010. In the liver of mice receiving injections of D-GalN/LPS, hepatocytes apoptosis and the infiltration of monocytes/macrophages were blocked by SKLB010. Furthermore, the survival rate of mice following D-GalN/LPS treatment was significantly improved by a single injection with SKLB010. In vivo, the luminescence intensity was suppressed by SKLB010 in NF-κB-luc mice after D-GalN/LPS treatment. In vitro, the production of tumor necrosis factor (TNF)-α and nitrite/nitrate in LPS-stimulated RAW264.7 macrophages was decreased by SKLB010 in a dose-dependent manner. Our further studies demonstrated that SKLB010 inhibited the phosphorylation of IκBα and p38MAPK, and the DNA binding activity of NF-κB in RAW264.7 cells. In conclusion, treatment with only a single injection of SKLB010 could significantly attenuate acute inflammation in mice induced by D-GalN/LPS, and these effects are likely associated with the inhibition of NF-κB activity. Copyright © 2014 Elsevier B.V. All rights reserved.

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出版当年[2014]版：

大类 | 3 区医学

小类 | 3 区药学 4 区免疫学

最新[2023]版：

大类 | 2 区

医学

小类 | 2 区免疫学 2 区药学

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第一作者机构： [1]State Key Laboratory of Biotherapy,West China Hospital, West China Medical School, Sichuan University, Chengdu, China

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通讯机构： [1]State Key Laboratory of Biotherapy,West China Hospital, West China Medical School, Sichuan University, Chengdu, China [*1]State Key Laboratory of Biotherapy, West China Hospital, West China Medical School, Sichuan University, Keyuan Road 4, Gaopeng Street, Chengdu, 610041, China

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