雨蛙素联合脂多糖致小鼠重症急性胰腺炎模型的建立及其机理的探讨

为建立一种快速、简便、无创伤性的小鼠重症急性胰腺炎模型。本实验运用雨蛙素联合脂多糖小鼠腹腔内给药;血淀粉酶和胰腺湿重测定;胰腺和胰外器官病理学检查;腺泡细胞透射电镜观察;血清NO浓度测定;胰腺组织SOD和MDA测定。结果发现,雨蛙素联合脂多糖组血淀粉酶、NO浓度和胰腺湿重均增高,SOD活力降低,MDA含量升高,胰腺间质水肿、实质出血坏死、炎症细胞浸润,腺泡细胞受损严重,胰外多器官受到不同程度的损害;雨蛙素组胰腺无明显出血坏死,胰外器官正常;脂多糖组胰腺基本正常,胰外器官轻微炎症浸润。由本实验结果显示,雨蛙素联合脂多糖致小鼠重症急性胰腺炎模型具有人类重症急性胰腺炎的病理特征,为非创伤性,成模快速稳定,重复性好;脂多糖促使雨蛙素诱导的急性水肿型胰腺炎重症化的机理与自由基释放-清除机制和氧化-抗氧化机制紊乱有关。

CREATE THE MOUSE MODEL OF SEVERE ACUTE PANCREATITIS INDUCED BY CAERULEIN PLUS LIPOPOLYSACCHARIDE AND STUDY ON ITS PATHOGENESIS

To set up a nontraumatic and convenient mouse model of severe acute pancreatitis (SAP). Caerulein(Cn) was injected the mice intraperitonealy with lipopolysaccharide(LPS). Serum amylase and pancreas weight were measured in experiment. The pathological changes of pancreas and other organs were observed under light microscope. The ultrastructure of acini were observed under transmission electron microscope (TEM). Serum NO concentration were measured and the SOD and MDA in pancreas were examined. The results in Cn+LPS group were showed that serum amylase, NO concentration and pancreas weight were increased, SOD deduced and MDA increased. Severe edema, inflammation infiltration, necrosis and different extent of hemorrhage were showed. The acini were damaged severely. And the lesion of other organs were also happened. In Cn group, there were only pancreatic interstitial edema but no parenchmal necrosis or hemorra-hage, and the other organs were normal. In LPS group, pancreas were almost normal and the organs besides pancreas were only showed light inflammation infiltration. The SAP mouse model induced by caerulein plus LPS has the same pathological characteristics of human SAP, which can be used in human SAP research. The unbalance of oxygen free radical release-elimination and oxidation-antioxidation mechanisms might be involved in the pathogenesis of mouse model of severe acute pancreatitis induced by intraperitoneal injection of caerulein plus LPS.