par Le Moine, Olivier 
;Louis, Hubert ;Stordeur, Patrick ;Collette, Jean Marie ;Goldman, Michel ;Devière, Jacques
Référence Gastroenterology, 113, 5, page (1701-1706)
Publication Publié, 1997-11
;Louis, Hubert ;Stordeur, Patrick ;Collette, Jean Marie ;Goldman, Michel ;Devière, Jacques Référence Gastroenterology, 113, 5, page (1701-1706)
Publication Publié, 1997-11
Article révisé par les pairs
| Résumé : | BACKGROUND & AIMS: Reactive oxygen intermediates and cytokines are key effectors in reperfusion injury after liver ischemia. We hypothesized that reactive oxygen intermediates act as a signal for the release of tumor necrosis factor (TNF) and interleukin 10 (IL-10) after reperfusion of cold-preserved livers. METHODS: An endotoxin-free isolated perfused mouse liver system was designed. Harvested mouse livers were stored at 4 degrees C for 0-28 hours and reperfused for 90 minutes with a warm oxygenated Hank's balanced salt solution (alone or with additives). Cytokine messenger RNA (mRNA) from whole liver was measured by reverse-transcription polymerase chain reaction. Cytokine protein levels and liver injury assessed by alanine aminotransferase levels were evaluated in liver effluent during reperfusion. RESULTS: TNF and IL-10 mRNA and protein concentrations were increased after reperfusion of ischemic livers. N-Acetylcysteine and allopurinol dramatically decreased TNF (-64% and -62%) and IL-10 (-49% and -57%) levels in the effluents, as did an inhibitor of the transcription factor NF-kappaB mobilization (-73% and -76% for TNF and IL-10, respectively). Liver injury was decreased by -40%, -43%, and -54% for the three inhibitors, respectively. CONCLUSIONS: Reactive oxygen intermediates are involved in TNF and IL-10 release after reperfusion of cold-preserved livers. |
