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

Abstract EN

Objective.

To investigate the role of oxidative stress, NF-κB 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-α, IL-6, SOD, MDA, ROS, NF-κB, and IκB-β were monitored by ELISA, biochemical methods, EMSA, and Western blot, respectively.

Results.

The plasma inflammatory mediators and the contents of MDA, ROS, and NF-κB 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 IκB-β 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 IκB-β protein.

Conclusion.

UTI can attenuate SI-OAI induced IMI via inhibition of NF-κB activity, subsequently inhibiting the expression of inflammatory cytokines and by combating oxidative stress.