Melatonin, the primary pineal hormone, has been reported to protect from oxidative injury after ischemia-reperfusion (IR). The aim of this study was to evaluate the effects of exogenous melatonin on intestinal integrity, ileal colonization, and bacterial translocation 45-minute after mesenteric IR. Sixteen male ACI rats randomly divided into two groups underwent 45-minutes intestinal ischemia by clamping the superior mesenteric artery. One hour prior to ischemia, study animals (n=8, group A) were treated with melatonin (10 mg/kg IP) while control animals (n=8, group B) received the same volume of saline solution. An additional six animals underwent laparotomy and served as a sham-operated group. Animals were sacrificed 24 hours after reperfusion; peritoneal swabs and biopsies of liver, spleen, lung, mesenteric lymph nodes, cecum, and terminal ileum were obtained for microbiology. The ileum samples were also processed for histopathological evaluation of IR-induced injury. Twenty-four hours after reperfusion bacterial translocation to the peritoneal cavity present in all group B animals was reduced to 37.5% among those that were melatonin-treated (group A; P <.05). Furthermore bacterial translocation to mesenteric lymph nodes, spleen, and liver was significantly lower in group A than group B (P <.05). Although cecal and ileal counts did not differ between the two groups, ileal counts from control animals showed increased colonization. Accordingly, a single injection of exogenous melatonin significantly reduced the intestinal IR injury and prevented bacterial translocation.

Sileri, P., Sica, G., Gentileschi, P., Venza, M., Benavoli, D., Jarzembowski, T., et al. (2004). Melatonin reduces bacterial translocation after intestinal ischaemia-reperfusion injury. TRANSPLANTATION PROCEEDINGS, 36(10), 2944-2946 [10.1016/j.transproceed.2004.10.085].

Melatonin reduces bacterial translocation after intestinal ischaemia-reperfusion injury

Sileri P.;Sica G;Gentileschi P.;Manzelli A.;
2004

Abstract

Melatonin, the primary pineal hormone, has been reported to protect from oxidative injury after ischemia-reperfusion (IR). The aim of this study was to evaluate the effects of exogenous melatonin on intestinal integrity, ileal colonization, and bacterial translocation 45-minute after mesenteric IR. Sixteen male ACI rats randomly divided into two groups underwent 45-minutes intestinal ischemia by clamping the superior mesenteric artery. One hour prior to ischemia, study animals (n=8, group A) were treated with melatonin (10 mg/kg IP) while control animals (n=8, group B) received the same volume of saline solution. An additional six animals underwent laparotomy and served as a sham-operated group. Animals were sacrificed 24 hours after reperfusion; peritoneal swabs and biopsies of liver, spleen, lung, mesenteric lymph nodes, cecum, and terminal ileum were obtained for microbiology. The ileum samples were also processed for histopathological evaluation of IR-induced injury. Twenty-four hours after reperfusion bacterial translocation to the peritoneal cavity present in all group B animals was reduced to 37.5% among those that were melatonin-treated (group A; P <.05). Furthermore bacterial translocation to mesenteric lymph nodes, spleen, and liver was significantly lower in group A than group B (P <.05). Although cecal and ileal counts did not differ between the two groups, ileal counts from control animals showed increased colonization. Accordingly, a single injection of exogenous melatonin significantly reduced the intestinal IR injury and prevented bacterial translocation.
Pubblicato
Rilevanza internazionale
Articolo
Esperti anonimi
Settore MED/18 - Chirurgia Generale
English
Con Impact Factor ISI
Animals; Bacterial Translocation; Disease Models, Animal; Intestines; Liver; Lung; Lymph Nodes; Male; Melatonin; Peritoneum; Rats; Rats, Inbred ACI; Reperfusion Injury; Spleen
Sileri, P., Sica, G., Gentileschi, P., Venza, M., Benavoli, D., Jarzembowski, T., et al. (2004). Melatonin reduces bacterial translocation after intestinal ischaemia-reperfusion injury. TRANSPLANTATION PROCEEDINGS, 36(10), 2944-2946 [10.1016/j.transproceed.2004.10.085].
Sileri, P; Sica, G; Gentileschi, P; Venza, M; Benavoli, D; Jarzembowski, T; Manzelli, A; Gaspari, Al
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/2108/197099
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