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c‐Jun N‐terminal kinase activation during warm hepatic ischemia/reperfusion injuries in a rat model
Author(s) -
Shinoda Masahiro,
Shimazu Motohide,
Matsuda Satoshi,
Wakabayashi Go,
Tanabe Minoru,
Hoshino Ken,
Kamei Shusaku,
Koyasu Shigeo,
Kitajima Masaki
Publication year - 2002
Publication title -
wound repair and regeneration
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.847
H-Index - 109
eISSN - 1524-475X
pISSN - 1067-1927
DOI - 10.1046/j.1524-475x.2002.t01-1-10507.x
Subject(s) - ischemia , medicine , reperfusion injury , tumor necrosis factor alpha , necrosis , kinase , pathology , biology , microbiology and biotechnology
Ischemia/reperfusion injuries are a major problem in liver resections and transplantations. Tumor necrosis factor‐α has been widely investigated as a key mediator in the mechanism of ischemia/reperfusion injury. Upstream signal transduction mechanisms for tumor necrosis factor‐α have not been well documented. Therefore, we assessed c‐Jun N‐terminal kinase activation during warm hepatic ischemia/reperfusion injuries in a rat model. Male Wistar rats were subjected to 30 minutes of ischemia followed by reperfusion. Hepatic enzymes, histological examinations, microfluorographs, and tumor necrosis factor‐α protein production (in the serum and liver tissue) were analyzed during the course of reperfusion. c‐Jun N‐terminal kinase activity was measured by a radioisotope kinase assay. Ischemia/reperfusion injuries were characterized by an elevation in hepatic enzyme, the histological degeneration of hepatocytes, and an increase in the number of nonviable cells. Moreover, increased endothelial‐adherent leukocytes and tumor necrosis factor‐α protein production were also observed. c‐Jun N‐terminal kinase activity at 60 minutes after reperfusion was 12.4 times higher than the pre‐ischemia level. These results suggest that c‐Jun N‐terminal kinase may play some role in the mechanism of ischemia/reperfusion injuries. (WOUND REP REG 2002;10:314–319)