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Issue 58, 2018, Issue in Progress
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SKLB023 protects mice against acute liver injury by inhibiting proinflammatory cytokine production in both T cells and macrophages

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Abstract

Acute liver failure is a severe clinical syndrome accompanied with excessive inflammatory response. Our previous study demonstrated that SKLB023, a novel thiazolidinedione derivative, showed potent anti-inflammatory activity in rheumatoid arthritis. The purpose of the present study is to evaluate the protective effect of SKLB023 on lipopolysaccharide (LPS)/D-GalN-induced liver failure and to explore the underlying molecular mechanisms. Our results showed that SKLB023 significantly improved mortality and liver injury as indicated by reduced serum levels of aminotransferases and alleviated pathological damage. Additionally, SKLB023 decreased the percentage of activated T cells and macrophages as well as the serum levels of cytokines in vivo. Furthermore, SKLB023 decreased levels of TNF-α and IL-6 secreted from liver macrophages (Kupffer cells) stimulated by LPS in vitro. Our results indicated that the protective effects of SKLB023 were associated with its significant impact on the inflammatory cytokines, which were produced by both T cells and macrophages.

Graphical abstract: SKLB023 protects mice against acute liver injury by inhibiting proinflammatory cytokine production in both T cells and macrophages

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Supplementary files

Article information


Submitted
01 May 2018
Accepted
14 Sep 2018
First published
27 Sep 2018

This article is Open Access

RSC Adv., 2018,8, 33338-33346
Article type
Paper

SKLB023 protects mice against acute liver injury by inhibiting proinflammatory cytokine production in both T cells and macrophages

J. Yu, L. Liu, H. Zhang, Y. Wu, H. Pei, L. Ma, A. Xiong and C. Xie, RSC Adv., 2018, 8, 33338
DOI: 10.1039/C8RA03720E

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    [Original citation] - Published by The Royal Society of Chemistry.

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