Mitogen-Activated Protein Kinases Are Activated in Placental Injury in Rat Model of Acute Pancreatitis in Pregnancy

Objectives: To establish a rat model of acute pancreatitis in pregnancy (APIP) and evaluate its general presentations, assess placental injury, and discuss possible mechanisms. Methods: The APIP rat model was induced by sodium taurocholate in Sprague-Dawley rats of later gestation. Normal and sham-operated (SO) rats in later gestation were set as controls, 3 time points were set in SO and APIP groups to determine optimal modeling time. Histological changes of pancreas and placenta were assessed. Placental injury was determined by immunohistochemistry stain of caspase-3. Serum levels of amylase, lipase, and Ca2+; proinflammatory cytokines as tumor necrosis factor-alpha, interleukin-1 beta (IL-1 beta), IL-6, and anti-inflammatory cytokine IL-10 by enzyme-linked immunosorbent assay; mitogen-activated protein kinases and their phosphorylated forms by Western blotting. Results: Pancreatic necrotizing and placental injury occurred in time-dependent patterns. Serum levels of amylase and lipase significantly increased but Ca2+ decreased; tumor necrosis factor-alpha, IL-1 beta, IL-6, and IL-10 were all increased in the APIP group; c-Jun N-terminal kinase, p38, and ERK1/2 were activated but with different distributing patterns in the placenta. Conclusions: Placental injury is involved in the rat model of APIP, and a modeling time of 6 hours is optimal and conducive to further studies; c-Jun N-terminal kinase and p38 may play important roles in placental injury during APIP.