Abstract

Aim: In this experimental study; the role of tumor necrosis factor alpha (TNF-a) which early mediator and high mobility group box-1 (HMG-1) which late mediator of the inflammation in the pathophysiology of the ileus and the effects of inhibition of this mediators were investigated on intestinal morphology and motility during peritonitis.

Materials and Methods: The rats were assigned four groups including eigth rat. While laparatomy was performed the control group only, cecal ligation and puncture was performed in the peritonitis after laparatomy. Etanercept (8 mg/kg.) was appied via intraperitoneal (‹P) injection in the etanercept group on the time of one and four hours after peritonitis. Etylpurivate was applied ‹P in fourth group on the time of 12 and 24 hours after peritonitis.Thirtysix hours later, tissue malondialdehyde and myeloperoxidase levels were measured in the ileal samples and TNF-a lewels were measured in the blood. In the histopathological evaluation; Chiu scor and semicantitative scor were used for ileal injury by light microscope. The ileal contractions were evaluated with electical field stimulation, potatium chlorur and carbacahol (CCh) in the organ bath.

Results: TNF-a levels that increased in the peritonitis group were significantly reduced in the etanercept group. Tissue MDA and MPO levels were reduced both etanercept and etylpurivate groups. It has been deternined that peritonitis caused seriosly inflammation and the tissue injury on the intestine and etanercept and etylpurivate applying significantly reduced this changes. When the electrical stimulation was given on the ileal samples, contractions were increased in the etanercept group. The contractions of the ileal samples were improved in the etylpurivate group with KCl, and in the etanercept group with cumulative CCh.

Conclusions: TNF-a and HMGB-1 have an important role on the intestinal injury and reduced motility with peritonitis. These data shown that both cytokine have effect by different mechanisms and path ways in this process. More studies to explain the mechanisms allow the inhibition of these cytokines could use the treatment in the future.