Jin Chang, Li Ji Cheng
Department of Lymphology, Institute of Cell Biology, Zhejiang University, Hangzhou 310031, China.
Shi Yan Sheng Wu Xue Bao. 2003 Apr;36(2):91-8.
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 hemorrhage, 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.
建立一种非创伤性且便捷的重症急性胰腺炎(SAP)小鼠模型。将小鼠腹腔注射雨蛙素(Cn)和脂多糖(LPS)。实验中检测血清淀粉酶和胰腺重量。在光学显微镜下观察胰腺及其他器官的病理变化。在透射电子显微镜(TEM)下观察腺泡的超微结构。检测血清NO浓度并检测胰腺中的超氧化物歧化酶(SOD)和丙二醛(MDA)。结果显示,Cn + LPS组血清淀粉酶、NO浓度和胰腺重量增加,SOD减少,MDA增加。出现严重水肿、炎症浸润、坏死及不同程度的出血。腺泡严重受损。其他器官也出现病变。在Cn组,仅出现胰腺间质水肿,无实质坏死或出血,其他器官正常。在LPS组,胰腺基本正常,除胰腺外的器官仅表现为轻度炎症浸润。雨蛙素加LPS诱导的SAP小鼠模型具有与人类SAP相同的病理特征,可用于人类SAP研究。腹腔注射雨蛙素加LPS诱导的重症急性胰腺炎小鼠模型的发病机制可能涉及氧自由基释放-清除和氧化-抗氧化机制的失衡。