Premium
Blockade of STAT3 does not alter acute injury after hepatic ischemia/reperfusion in mice
Author(s) -
Clarke Callisia Nathelee,
Tevar Amit,
Edwards Michael,
Lentsch Alex B
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.982.5
Subject(s) - stat3 , blockade , ischemia , reperfusion injury , medicine , liver injury , pharmacology , phosphorylation , ischemic preconditioning , chemistry , receptor , biochemistry
Background STAT3 is a critical transcription factor regulating the protective effects of liver ischemic preconditioning. However, its role in hepatic ischemia/reperfusion (I/R) injury is unclear. Here we investigated whether blockade of STAT3 phosphorylation altered the injury response to hepatic I/R injury. Methods Mice were subjected to 90 minutes of hepatic ischemia followed by reperfusion with or without ip injection of 5mg/kg AG490 (selective JAK2 inhibitor) or 10mg/kg of Stattic (direct inhibitor of STAT3 phosphorylation). Mice were sacrificed at 24 hr post reperfusion and liver injury (serum ALT), histology and tissue neutrophil accumulation (liver MPO) measured. Results Neither Stattic nor AG490 had any effect on liver injury induced by I/R. However, Stattic significantly reduced neutrophil accumulation. Conclusion The data suggest that STAT3 is not relevant to acute liver injury after I/R. However, it may be involved in pathways leading to recruitment of neutrophils.