Differential JNK, p38 and ERK response to renal injury in a rat model of acute pancreatitis in pregnancy.

OBJECTIVE

The objective of this study was to determine the mechanism of acute renal injury (ARI) in acute necrotizing pancreatitis in late pregnancy (ANPIP).

METHODS

Pregnant Sprague-Dawley rats in the third trimester were used for this study, and an ANPIP model was induced by injecting 5% sodium taurocholate into the biliary pancreatic duct. The rats were randomly divided into three groups: the normal, sham-operated (SO) and acute necrotizing pancreatitis (ANP) groups. Rats were killed at 3, 6, 12 h after the operation, and blood, pancreatic and renal tissue samples were harvested. Differences were detected in the physiology, pathology and cellular and molecular responses among the different groups.

RESULT: Serum amylase, lipase, urea and Cr levels were increased in rats with ANPIP. Additionally, expression of phosphorylation p38 and JNK as well as TNF-α and NF-κB were increased in the renal tissues of rats with ANPIP. The expression of phosphorylation ERK was decreased in the renal tissues of rats with ANPIP.

CONCLUSIONS

Mitogen-activated protein kinases may play an important role in renal injury in rat models of ANPIP.