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Gastroenterology Research and Practice
Volume 2014 (2014), Article ID 858237, 9 pages
Research Article

Urinary Trypsin Inhibitor Ameliorates Seawater Immersion-Induced Intestinal Mucosa Injury via Antioxidation, Modulation of NF-B Activity, and Its Related Cytokines in Rats with Open Abdominal Injury

1Department of General Surgery, The 175th Hospital of PLA, Southeast Hospital Affiliated to Xiamen University, No. 269 Zhanghua Middle Road, Zhangzhou, Fujian 363000, China
2The First College of Clinical Medical Science, China Three Gorges University, No. 183 Yiling Road, Yichang, Hubei 443000, China

Received 16 April 2014; Accepted 25 July 2014; Published 21 August 2014

Academic Editor: Paolo Gionchetti

Copyright © 2014 Xing Jian Zhang 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.


Objective. To investigate the role of oxidative stress, NF-B activity, and its related cytokines in the pathogenesis of seawater immersion after open abdominal injury (SI-OAI) and whether UTI treatment can attenuate SI-OAI induced IMI. Methods. Wistar rats were randomly divided into three groups: C group, S group, and U group. The rats in C group only suffered from anesthesia and surgical operation, whereas the rats in S group and U group received caudal vein injection of normal saline without/with 50,000 U/kg body weight of UTI. The activities of TNF-, IL-6, SOD, MDA, ROS, NF-B, and IB- were monitored by ELISA, biochemical methods, EMSA, and Western blot, respectively. Results. The plasma inflammatory mediators and the contents of MDA, ROS, and NF-B in intestine as well as the pathological scores in ileal mucosa were significantly increased in rats after SI-OAI, accompanied by a reduction in SOD activities and IB- levels. UTI treatment significantly attenuated intestinal histopathological changes with evidence of a decrease in all of the parameters, except for upregulation of the levels of SOD and IB- protein. Conclusion. UTI can attenuate SI-OAI induced IMI via inhibition of NF-B activity, subsequently inhibiting the expression of inflammatory cytokines and by combating oxidative stress.