急性胰腺炎时胰腺组织修复机制的研究  

A study on mechanism of repair of pancreas after acute pancreatitis

作　　者：张雁[1] 李非[1] 张淑文[1] 崔叶青[1] 孙海晨[1] 孙家邦[1] 

机构地区：[1]首都医科大学宣武医院普通外科,北京市100053

出　　处：《中华肝胆外科杂志》2005年第5期324-327,共4页Chinese Journal of Hepatobiliary Surgery

基　　金：北京市重点学科资金资助(卫科扶字11号)

摘　　要：目的探讨急性胰腺炎后胰腺修复的机制。方法实验所用动物为NIH Swiss小鼠,分两组,分别是盐水对照组、急性胰腺炎组(AP组)。急性胰腺炎诱导采用蛙皮素腹腔注射,用常规病理评价胰腺的炎症程度;流式细胞仪检测细胞增殖状态;免疫组化方法检测胶原Ⅰ的表达,蛋白酶谱检测MMP-3的表达。结果病理检测结果:蛙皮素腹腔注射可诱导小鼠急性胰腺炎。在急性胰腺炎组小鼠AP诱导后8 h胰腺组织损伤最严重,至第7天时组织损伤基本恢复正常。胰腺流式细胞仪检测发现AP诱导后细胞增殖状态分三个时期:早期的增殖活跃期、中期的增殖抑制期和后期的高增殖状态。胶原Ⅰ的检测显示:盐水对照组胶原Ⅰ有少量表达,AP时胶原Ⅰ表达增强。MMP-3的检测结果:盐水对照组基本无表达,在AP时酶的活性增高。结论急性胰腺炎后,胰腺组织可进行修复。在其修复过程中,既有组织细胞的增殖修复,又存在间质纤维化修复和塑性。Objective To study the mechanism of repair of pancreas after acute pancreatitis(AP).Methods NIH Swiss mice were randomized into the saline control group and AP group.AP was induced by intraperitoneal injection of 50 ug/kg body weight cearulein for 4 times,once per hour.The cellular proliferation was detected using flow cytometry.Collagen I was detected with immunohistochemistry.Protein zymography was used to evaluate the expression of matrix metalloproteinase-3(MMP-3).Results In the AP group,the pancreatic lesions were the severest in 8 h and then recovered on the 7th d after induction of AP.Flow cytometry showed that there were three stages of cell proliferation after AP: the active proliferation in early stage,inhibition of proliferation in middle stage and high proliferation in the late stage.The expression level of collagen I and MMP-3 was markedly higher in the AP group than in the saline control group.Conclusions The pancreas can be repaired after AP.The regeneration mechanism includes interstitial fibrosis and acinar cell replication.

关 键 词：急性胰腺炎 胰腺组织 修复机制 流式细胞仪检测 细胞增殖状态 MMP-3 免疫组化方法 腹腔注射 检测结果 组织损伤 间质纤维化 胶原Ⅰ 对照组 胰腺修复 炎症程度 酶谱检测 增殖抑制 表达增强 活性增高 修复过程 组织细胞 蛙皮素 

分 类 号：R576[医药卫生—消化系统] R45[医药卫生—内科学]