中文摘要：

目的建立一种稳定的胰腺炎并脑损伤模型,以进一步探讨胰腺炎脑损伤的机制。方法24只成年雄性SD大鼠,随机分为假手术（sham operation,SO）组,重症急性胰腺炎（SAP）组和胰蛋白酶制模组（trypsin）,每组8只大鼠。各组大鼠均于制模后12 h采集脑组织和胰腺组织标本。比较各组大鼠的死亡率;采用酶联免疫吸附试验（enzymelinked immunosorbent assay,ELISA）测定血清细胞间紧密连接蛋白（Zo-1）含量;透射电镜观察脑组织超微结构变化;HE染色观察脑组织病理学变化。结果SAP组大鼠死亡率较trypsin组明显升高,SO组无大鼠死亡;SAP组Zo-1水平均明显高于SO组（P〈0.05）,trypsin组Zo-1水平与SAP组呈现一致性变化（P〉0.05）。SAP组和trypsin组均出现明显神经元细胞肿胀、毛细血管淤血、血管通透性增加、血栓形成、线粒体肿胀和细胞凋亡等超微结构的变化。结论胰蛋白酶可能为SAP脑损伤的元凶;用胰蛋白酶制备SAP模型大鼠死亡率低,为进一步研究脑损伤的机制和进行相关治疗研究提供了稳定的动物模型。

英文摘要：

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.