Transplantologiya 2014

Figure 4. Photomicrograph. The strangulated ileum wall of the animals from experimental group III: Preserved intestinal mucosal structures as a result of intravenous Prx VI administration (H&E stain, x200).
Discussion

An organ I/R injury is a multifactorial pathological process. The reperfusion of the ischemic bowel is associated with dramatic consequences causing the production of reactive oxygen species and a powerful oxidative stress [8, 16]. The oxidative stress developing after a resolved strangulation constitutes an important link in the pathogenesis of subsequent injury to the small intestine [17].

In our study, we investigated the effect of antioxidant enzyme Prx VI on the consequences of reperfusion in the ischemia-affected small intestine.

The study has demonstrated that a 60-minute strangulation of a small intestine loop in a rat followed by the reintroduction of the main blood flow for 120 minutes leads to destructive morphological changes of the intestinal wall, mainly affecting the intestinal mucosa. This is consistent with the literature reports showing that a small intestine reperfusion following the resolution of strangulated ileum is accompanied by a further development of necrobiotic disorders and necrotic lesions in the intestinal mucosa with progressing disintegration of the simple columnar epithelium [17]. Within two hours of reperfusion period, the pathomorphologic changes in the intestine reach their maximum.

In our study we have found that the administration of Prx VI in a rat may protect the intestine from I/R-injury. In the intestines of the animals who received Prx VI, the intestinal mucosa structure and the villi-crypt integrity were preserved. Thus, exogenous Prx VI prevents a massive loss of ileal cells in a rat protecting the tissue against destructive effects of reactive oxygen species. Worthwhile mentioning, the Prx VI has been found in all mammalian cells and detected in the largest amounts in the epithelial tissues of the lungs, respiratory tract, gastrointestinal tract, and oral cavity [18]. Although mammalian Prx VI gene expression has been shown to be regulated by an oxidative stress [20], probably, a proper endogenous Prx VI activity appears insufficient to neutralize the oxidative stress in I/R. In this case, a significant increase of Prx in the tissue of the small intestine achieved by its administration into the bloodstream might have controlled the oxidative stress at a safe level.

A protective effect of exogenous Prx VI on epithelial tissue has been shown in various organ lesions. Applying Prx VI directly on the tracheal mucosa of a rat after thermal and/or chemical burns of the upper respiratory tract significantly preserves epithelial cells and promotes regenerative processes [10-12], and also markedly accelerates the healing of cut wounds [14]. In this paper we have shown a protective effect of peroxiredoxins on the strangulated small intestine.