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World J Gastroenterol. Aug 14, 2013; 19(30): 4925-4934
Published online Aug 14, 2013. doi: 10.3748/wjg.v19.i30.4925
Published online Aug 14, 2013. doi: 10.3748/wjg.v19.i30.4925
Tumor necrosis factor-α mediates JNK activation response to intestinal ischemia-reperfusion injury
Qi Yang, Feng-Ping Zheng, Ya-Shi Zhan, Jin Tao, Si-Wei Tan, Hui-Ling Liu, Bin Wu, Department of Gastroenterology, the Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510630, Guangdong Province, China
Author contributions: Yang Q and Zheng FP contributed equally to this work; Yang Q, Zheng FP and Wu B designed the research; Yang Q, Zheng FP, Zhan YS, Tao J, Tan SW, Liu HL and Wu B performed the research and analyzed the data; and Yang Q and Wu B wrote the paper.
Supported by Grants-in-Aid from the Major Projects Incubator Program of the National Key Basic Research Program of China, No. 2012CB526700; National Natural Science Foundation of China, No. 30971357; Natural Science Foundation of Guangdong Province, No. S2011020002348; Science and Technology Planning Project of Guangdong Province, No. 2009B060300001; and Major Projects Incubator Program of Sun Yat-Sen University, No. 10ykjc25
Correspondence to: Bin Wu, MD, PhD, Professor, Department of Gastroenterology, the Third Affiliated Hospital of Sun Yat-Sen University, 600 Tianhe Road, Guangzhou 510630, Guangdong Province, China. binwu001@hotmail.com
Telephone: +86-20-85253095 Fax: +86-20-85253336
Received: March 13, 2013
Revised: May 31, 2013
Accepted: June 19, 2013
Published online: August 14, 2013
Processing time: 153 Days and 12 Hours
Revised: May 31, 2013
Accepted: June 19, 2013
Published online: August 14, 2013
Processing time: 153 Days and 12 Hours
Core Tip
Core tip: Ischemia-reperfusion (I/R) injury is a critical physiopathological phenomenon wherein further damage may occur when the blood supply of ischemic organs is recovered, and the mechanism of I/R remains unclear. This paper demonstrates that tumor necrosis factor-α (TNF-α) played a pivotal role in intestinal I/R injury, and pretreatment with the TNF-α inhibitor pentoxifylline or the TNF-α antibody infliximab remarkably attenuated I/R-induced injury by inhibiting TNF-α-mediated apoptosis and c-Jun N-terminal kinase (JNK) activation. The results of the study indicate there is a TNF-α-mediated JNK activation response to intestinal I/R injury.