Abstract:

BACKGROUND: As JNK kinase inhibitor, SP600125 can specific and selective block JNK signal transduction pathways. However, it is poorly understood the role of SP600125 on hepatic ischemia/reperfusion (IR) injury.
OBJECTIVE: SP600125 was used to interfere in hepatic IR injury and to analyze the mechanism of JNK signaling pathway in this process.
METHODS：Thirty normal male Sprague-Dawley rats were randomly divided into sham operation group, IR group and JNK inhibitor SP600125 group. The left medius lobe was blocked in the IR group. At half hour before operation, 15 mg/kg SP600125 were injected into rats in the SP600125 group. All rats were killed at 2 hours after reperfusion. Routine assays were performed for testing the levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST); the pathological changes in the liver was evaluated with hematoxylin-eosin staining and contents of maleicdialdehyde (MDA) and myeloperoxidase (MPO) in liver tissues were detected by colorimetric method.
RESULTS AND CONCLUSION: Compared to the IR group, the levels of serum ALT, AST, contents of MPO and MDA, as well as expression of p-JNK in hepatic tissues decreased significantly in the SP600125 group. The pathological changes of hepatic IR injury could be alleviated obviously. The activation of JNK signal pathway plays a pivotal role in hepatic IR injury, which can be alleviated by SP600125 treatment.