These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Reduced hepatic ischemia/reperfusion injury by IL-4: potential anti-inflammatory role of STAT6.
    Author: Kato A, Yoshidome H, Edwards MJ, Lentsch AB.
    Journal: Inflamm Res; 2000 Jun; 49(6):275-9. PubMed ID: 10939617.
    Abstract:
    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.
    [Abstract] [Full Text] [Related] [New Search]