Zhang X, Jiang W, Zhou AL, Zhao M, Jiang DR. Inhibitory effect of oxymatrine on hepatocyte apoptosis via TLR4/PI3K/Akt/GSK-3β signaling pathway. World J Gastroenterol 2017; 23(21): 3839-3849 [PMID: 28638224 DOI: 10.3748/wjg.v23.i21.3839]
Corresponding Author of This Article
Dr. Dao-Rong Jiang, Department of Infectious Diseases, Affiliated Hospital of Nantong University, No. 20, Xisi Road, Nantong 226001, Jiangsu Province, China. jdr@ntu.edu.cn
Research Domain of This Article
Medicine, Research & Experimental
Article-Type of This Article
Basic Study
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Gastroenterol. Jun 7, 2017; 23(21): 3839-3849 Published online Jun 7, 2017. doi: 10.3748/wjg.v23.i21.3839
Inhibitory effect of oxymatrine on hepatocyte apoptosis via TLR4/PI3K/Akt/GSK-3β signaling pathway
Xian Zhang, Wei Jiang, Ai-Ling Zhou, Min Zhao, Dao-Rong Jiang
Xian Zhang, Dao-Rong Jiang, Department of Infectious Diseases, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China
Wei Jiang, Department of Science Technology and Industry, Nantong University, Nantong 226019, Jiangsu Province, China
Ai-Ling Zhou, Department of Pathophysiology, Medical School of Nantong University, Nantong 226001, Jiangsu Province, China
Min Zhao, Department of Pathology, Nantong Tumor Hospital, Nantong 226000, Jiangsu Province, China
Author contributions: Zhang X and Jiang W contributed equally to this work; Zhang X and Jiang W designed the study, performed the experiments and wrote the manuscript; Zhou AL and Zhao M analyzed the data; Jiang DR helped to review and edit the manuscript.
Supported bythe Jiangsu Bureau of Traditional Chinese Medicine, No. YB2015177.
Institutional review board statement: The study was reviewed and approved by the Laboratory Animal Center of NTU.
Conflict-of-interest statement: We declare that there are no conflicts of interest.
Data sharing statement: No additional data are available.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Dr. Dao-Rong Jiang, Department of Infectious Diseases, Affiliated Hospital of Nantong University, No. 20, Xisi Road, Nantong 226001, Jiangsu Province, China. jdr@ntu.edu.cn
Telephone: +86-13606299378 Fax: +86-513-85052085
Received: December 1, 2016 Peer-review started: December 6, 2016 First decision: January 19, 2017 Revised: February 9, 2017 Accepted: March 2, 2017 Article in press: March 2, 2017 Published online: June 7, 2017 Processing time: 187 Days and 8.2 Hours
Core Tip
Core tip: The role of oxymatrine (OMT) in inhibiting apoptosis in acute liver failure (ALF) was investigated. OMT pretreatment protected liver cells by improving the liver pathological change and reducing serum aminotransferase in lipopolysaccharide/D-galactosamine-induced ALF in rats. OMT preconditioning down-regulated apoptosis of hepatocytes and ameliorated pathological changes in liver tissue. The levels of alanine aminotransferase, aspartate aminotransferase, tumor necrosis factor-α and interleukin-1β in the model group increased significantly, and were significantly reduced by OMT pretreatment. OMT pretreatment down-regulated expression of Toll-like receptor (TLR)4 and active caspase-3 and the Bax/Bcl-2 ratio, and up-regulated expression of P-AKTSer473 and P-GSK3βSer9. OMT could inhibit hepatocyte apoptosis through the TLR4/PI3K/Akt/GSK-3β signaling pathway.
