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Mediators of Inflammation
Volume 2018, Article ID 7859601, 11 pages
Research Article

The Protective Mechanism of CAY10683 on Intestinal Mucosal Barrier in Acute Liver Failure through LPS/TLR4/MyD88 Pathway

1Department of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, China
2Hubei Provincial Center for Disease Control and Prevention, Wuhan, China

Correspondence should be addressed to Zuo-Jiong Gong; moc.361@gnogjz

Received 30 October 2017; Revised 30 December 2017; Accepted 11 January 2018; Published 13 March 2018

Academic Editor: Fabio S Lira

Copyright © 2018 Yao Wang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The purpose of this study was to investigate the protective mechanism of HDAC2 inhibitor CAY10683 on intestinal mucosal barrier in acute liver failure (ALF). In order to establish ALF-induced intestinal epithelial barrier disruption models, D-galactosamine/LPS and LPS were, respectively, used with rats and NCM460 cell and then administrated with CAY10683. Transepithelial electrical resistance (TEER) was measured to detect the permeability of cells. Real-time PCR and Western blotting were employed to detect the key mRNA and protein levels. The intestinal epithelial tissue pathology was detected. After interfering with CAY10683, the mRNA and protein levels of TLR4, MyD88, TRIF, and TRAF6 were decreased compared with model group (), whereas the levels of ZO-1 and occluding were elevated (). The permeability was elevated in CAY10683-interfered groups, when compared with model group (). And the degree of intestinal epithelial tissue pathological damage in CAY10683 group was significantly reduced. Moreover, CAY10683 significantly decreased the TLR4 staining in animal tissue. The HDAC2 inhibitor CAY10683 could promote the damage of intestinal mucosal barrier in ALF through inhibiting LPS/TLR4/MyD88 pathway.