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Interleukin‐10 suppresses hepatic ischemia/reperfusion injury in mice: Implications of a central role for nuclear factor κB
Author(s) -
Yoshidome Hiroyuki,
Kato Atsushi,
Edwards Michael J.,
Lentsch Alex B.
Publication year - 1999
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.510300120
Subject(s) - proinflammatory cytokine , reperfusion injury , chemokine , tumor necrosis factor alpha , cytokine , medicine , immunology , ischemia , transcription factor , inflammation , endocrinology , biology , biochemistry , gene
Abstract Ischemia/reperfusion injury of the liver requires the participation of proinflammatory cytokines, chemokines, and adhesion molecules, many of which are regulated by the transcription factor nuclear factor κB (NFκB). The anti‐inflammatory cytokine, interleukin‐10 (IL‐10) affects inflammatory reactions, at least in part, through inhibitory effects on the transcription factor, NFκB. The objective of the current study was to determine whether IL‐10 could suppress hepatic ischemia/reperfusion‐induced NFκB activation and the ensuing inflammatory liver injury. C57BL/6 mice underwent partial hepatic ischemia and reperfusion with or without intravenous injections of recombinant murine IL‐10. Hepatic NFκB activation was induced in a time‐dependent fashion. IL‐10 suppressed NFκB activation as well as messenger RNA expression of tumor necrosis factor‐α (TNF‐α) and macrophage inflammatory protein‐2 (MIP‐2). In addition, IL‐10 reduced serum levels of TNF‐α and MIP‐2. Hepatic neutrophil recruitment, liver edema, and hepatocellular injury were all significantly reduced by IL‐10. The data suggest that IL‐10 protects against hepatic ischemia/reperfusion injury by suppressing NFκB activation and subsequent expression of proinflammatory mediators.