Establishment of a new brain injury model with pancreatitis / 西安交通大学学报(医学版)

ABSTRACT

Objective To establish a stable brain injury model with pancreatitis and explore the mechanism of brain injury resulting from severe acute pancreatitis (SAP) in experimental rat models. Methods Twenty-four adult male Sprague-Dawley rats were randomly divided into three groups sham operation (SO) group, SAP group and trypsin group, with eight rats in each. Brain tissue and pancreas tissue specimens were collected at 12 h after treatment. Death rate in each group was evaluated; the level of tight junction protein zonula occludens 1 (Zo-1) was determined by enzyme-linked immunosorbent assay. The ultrastructure of the brain tissues was examined using transmission electronic microscope; pathological changes in the brain tissues were observed with HE staining. Results The death rate was increased significantly in SAP group compared with that in trypsin group; no rats in SO group died. Zo-1 level was obviously lower in SO group than in SAP group and trypsin group (P<0.05). The ultrastructural changes were seen in the latter two groups, including obvious neuronal cell swelling, capiliary stasis, increased vascular permeability, thrombosis and cell apoptosis. Conclusion Trypsin may cause brain injury with pancratitis. The death rate of SAP model established by trypsin was low. We have provided a stable animal brain injury model for further study and treatment of brain injury.