论文部分内容阅读
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 investigate the mechanism of pancreatic repair after acute pancreatitis. Methods The NIH Swiss mice were divided into two groups: saline control group and acute pancreatitis group (AP group). Acute pancreatitis was induced by intraperitoneal injection of bombesin, and the degree of inflammation of the pancreas was evaluated by routine pathology. Cell proliferation was detected by flow cytometry. The expression of collagen Ⅰ was detected by immunohistochemistry and the expression of MMP-3 was detected by protease. Results Pathological examination results: Bombes injection of intraperitoneal injection can induce acute pancreatitis in mice. In the acute pancreatitis group, the pancreatic tissue injury was the most serious at 8 h after AP induction, and the tissue damage returned to normal on the 7th day. Pancreatic flow cytometry found that AP induced cell proliferation status after three periods: early proliferation active phase, the mid-term inhibition of proliferation and the late high proliferation state. Collagen Ⅰ test showed: saline control group collagen I expression, AP collagen Ⅰ enhanced expression. MMP-3 test results: saline control group was almost no expression, the enzyme activity in the AP increased. Conclusion Pancreatic tissue can be repaired after acute pancreatitis. In its repair process, both the proliferation of tissue cells repair, there are interstitial fibrosis repair and plasticity.