摘要
目的胰腺纤维化是慢性胰腺炎的主要病理特征,由于缺乏重复性好的研究模型,胰腺纤维化的发生、发展过程尚不清楚。本研究采用CCK类似物蛙皮素反复诱致大鼠胰腺炎,旨在探讨胰腺纤维化发生的分子机制。方法SD大鼠腹腔注射蛙皮素50μg/kg,每周3次,分别于第2周、第4周和第8 周处死大鼠,采用HE染色和VG胶色观察不同时期胰腺病理组织学变化和结缔组织增生情况。同时,采用RT-PCR法检测胰腺Colα1(Ⅰ)mRNA的表达水平。结果造模第2周和第4周,胰腺间质中可见明显的炎性细胞浸润;第8周,“管状复合体”形成,间质纤维结缔组织大量增生并向小叶内伸展,胶原纤维交织成网状;而且随着造模时间的延长,Colα1(Ⅰ)基因的表达逐渐上调。结论蛙皮素多次大剂量腹腔注射致反复急性胰腺炎发作可以诱导大鼠产生胰腺纤维化,Colα1(Ⅰ)mRNA水平随造模时间延长逐渐升高,其机制可能与细胞信号分子介导的胰腺星状细胞活化而发生表型转化有关。
Objective Pancreatic fibrosis is a major pathologic characteristic of chronic pancreatitis, As there is a lack of a reproducible model, early development and progression of pancreatic necrosis are poorly understood. We have developed a model of hyperstimulation pancreatitis with caerulein to better define the mechanisms of pancreatic fibrogenesis. Methods SDrats were used and caerulein （50 μg/kg） was injected into the peritoneal cavity 3 times per week. Animals were killed at 2. 4 and 8 weeks. Pancreata were prepared for hematoxylin and eosin（HE） staining and van Gieson staining during different periods. Meanwhile. the expression of Colal（ Ⅰ ）mRNA was detected by RTPCR. Results Microscopically, inflammatory cell infiltration and interstitial edema were observed at 2 weeks; mononuclear cell infiltration was observed at 4 weeks, and at 8 weeks interstitial fibrosis and tubular complex with dilated ducts were observed. Furthermore, the expression of Colal（ Ⅰ）mRNA increased with lapse of the observation period. Conclusions The findings suggest that the caerulein induced rat pancreatitis model is useful for study of eeiiular interactions and mediators involved in the activation of pancreatic stellate cells and the development of pancreatic fibrosis in vivo.
出处
《胰腺病学》
CAS
2005年第3期158-161,共4页
Chinese JOurnal of Pancreatology
基金
湖北省教育厅重点科研项目(2004X032)
