SP600125, a selective JNK inhibitor, aggravates hepatic ischernia-reperfusion injury
- Authors
- Lee, KH[Lee, Kyung-Hoon]; Kim, SE[Kim, Sang-Eun]; Lee, YS[Lee, Yun-Song]
- Issue Date
- 31-Aug-2006
- Publisher
- KOREAN SOC MED BIOCHEMISTRY MOLECULAR BIOLOGY
- Citation
- EXPERIMENTAL AND MOLECULAR MEDICINE, v.38, no.4, pp.408 - 416
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- EXPERIMENTAL AND MOLECULAR MEDICINE
- Volume
- 38
- Number
- 4
- Start Page
- 408
- End Page
- 416
- URI
- https://scholarworks.bwise.kr/skku/handle/2021.sw.skku/86877
- ISSN
- 1226-3613
- 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.
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Collections - Medicine > Department of Medicine > 1. Journal Articles
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