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Reduced hepatic ischemia/reperfusion injury by IL-4: potential anti-inflammatory role of STAT6
A Kato1, H Yoshidome, M J Edwards
1Department of Surgery, University of Louisville School of Medicine, J. G. Brown Cancer Center, Kentucky 40202, USA.
Objective And Design:
The ability of interleukin-4 (IL-4) to modulate activation of the transcription factors, NF-kappaB and STAT6, reduce proinflammatory cytokine expression and protect against liver injury induced by ischemia/reperfusion was assessed.
Materials And Subjects:
C57BL/6 mice underwent 90 minutes of partial hepatic ischemia followed by 1 or 8 h of reperfusion with or without intravenous administration of 1 microg (0.5 microg just prior to ischemia, 0.5 microg at reperfusion) recombinant murine IL-4. Liver expression of TNFalpha mRNA was determined by RT-PCR. Activation of NF-kappaB and STAT6 in liver nuclear extracts was assessed by mobility shift assay.
Results:
Hepatic ischemia/reperfusion increased hepatic expression of tumor necrosis factor-alpha (TNFalpha), induced significant neutrophil accumulation and liver injury. Treatment with IL-4 greatly suppressed liver TNFalpha mRNA expression, neutrophil accumulation and liver injury. IL-4 had no effect on liver NF-kappaB activation, but greatly increased the activation of STAT6.
Conclusions:
The data suggest that STAT6 activation by IL-4 may be responsible for the protective effects of this cytokine.
