[PDF][PDF] Interleukin‐10 suppresses hepatic ischemia/reperfusion injury in mice: Implications of a central role for nuclear factor κB

H Yoshidome, A Kato, MJ Edwards, AB Lentsch - Hepatology, 1999 - Wiley Online Library
H Yoshidome, A Kato, MJ Edwards, AB Lentsch
Hepatology, 1999Wiley Online Library
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 …
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.
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