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Exp Mol Med. 2006 Aug 31;38(4):408-16.

SP600125, a selective JNK inhibitor, aggravates hepatic ischemia-reperfusion injury.

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1
Department of Molecular and Cellular Biology, Sungkyunkwan University School of Medicine, Suwon 440-746, Korea.

Abstract

c-Jun N-terminal kinase (JNK) is activated during hepatic reperfusion, and JNK inhibitors are known to protect other major organs from ischemia-reperfusion (I/R) injury. We attempted to determine the effect of SP600125, a JNK inhibitor, on hepatic I/R injury using a partial ischemia model in mice. Compared to a vehicle-treated group, the SP600125- treated group showed a greater increase in serum ALT levels 24 h after reperfusion with more severe parenchymal destruction and leukocyte infiltration. Similarly, tissue myeloperoxidase and malondialdehyde levels were higher in the SP600125-treated group, and chemokine expression was also higher in the SP600125-treated group. These data, which are contradictory to previous results, indicate that JNK inhibition by SP600125 may be harmful in hepatic I/R injury. Therefore, care must be taken when investigating the therapeutic use of JNK inhibitors in hepatic I/R injury, especially in the context of the effects of JNK inhibition on inflammatory infiltration.

PMID:
16953120
DOI:
10.1038/emm.2006.48
[Indexed for MEDLINE]
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