急性结肠炎大鼠胃肠动力改变与ICC破坏有关研究  

作　　者：范玲 吴东方[2] 刘殿雷[3] 

机构地区：[1]杭州钢铁集体公司职工医院儿科,310007 [2]温州医学院组胚教研室,325000 [3]杭州市中医院外一科,310007

出　　处：《浙江临床医学》2016年第12期2202-2204,共3页Zhejiang Clinical Medical Journal

基　　金：浙江省中医药管理局优秀青年基金项目（2013ZQ026）;杭州市科技发展计划项目（20140733Q34）

摘　　要：目的在大鼠结肠炎模型基础上，初步探讨炎性肠病大鼠胃肠动力障碍的可能机制。方法将40只SD大鼠随机分成对照组和急性结肠炎组。肠炎组采用乙酸灌肠法制备，造模第3天，两组均禁食24h，次日经口灌入印度墨汁，麻醉后剖腹取出贵门至直肠末端快速测量墨汁在胃肠道的推进长度及胃肠道全长的长度，计算胃肠传输速率；用透射电镜观察远端结肠Cajal间质细胞（ICC）的超微结构变化；采用Weston Blot方法检测ICC膜上c-kit蛋白表达。结果与对照组比较，肠炎组胃肠传输速度明显减慢（P〈0．05）；电镜下，对照组远段结肠肌层超微结构为ICC呈纺锤形，有巨大的卵圆形核及向外伸展的长突起，胞质内有丰富的线粒体、大量的内质网，ICC与肠神经元及平滑肌细胞之间紧密联系；而肠炎组远端结肠肌层中ICC体积增大，胞质内线粒体肿胀、部分线粒体空泡样变，溶酶体数目增多，出现次级溶酶体内质网扩张，ICC与神经细胞及平滑肌间连接松散；Western blot分析结果显示，与对照组比较，肠炎组远端结肠ICC c-kit蛋白质的表达量显著降低（P〈0．05）。结论炎性肠病可导致胃肠动力障碍，其机制与ICC的破坏有关。Objective To preliminarily study the possible mechanism of disorder intestinal motility of acute colitis based on the model of SD rats with acute colitis. Methods 40 rats were randomly divided into control group and acute colitis group. The model of acute colitis rats was built by clyster with acetic acid. Three days later, both groups of rots were were fasted for 24 hours, and the next day 0.5 mL India ink were poured into orally. 30 min later, the rats were anesthetized, then we cut into the abdomen to get the whole digestive tube from cardia to the terminal rectum and quickly measured the ink promoting length in the gastrointestinal tract and the length of the whole gastrointestinal tract to calculate their ratio to get the rate of gastrointestinal transit. Electron microscopy was used to observe the ultrastructural changes of interstitial cells of Cajal （ ICC ） . Western blot analysis was used to detect the expression of c-kit protein on the membranes of ICC. Results Compared to rats in control group, the rate of gastrointestinal transit in rats with acute colitis significantly decreased （P〈0.05 ） . Under electron microscope, ultrastructure of interstitial cells of Cajal in muscle of distal colon of control rats was like the spindle, containing a huge oval nucleus and long processes stretching out, and the cytoplasm is rich in mitochondria, a large number of endoplasmic reticulum. Cell links was close among ICC, intestinal neurons and smooth muscle cells. While in acute colitis group, the volume of ICC in the distal colon muscle layer increased, swollen mitochondria in the cytoplasm, some mitochondria vacuolar degeneration, increased numbers of lysosomes and endoplasmie reticulum expansion in secondary lysosomes. The loose cell link among ICC, intestinal neurons and smooth muscle cells was observed. Western blot analysis revealed thatbut c-kit protein expression in ICC in distal colon tissues in acute colitis group was significantly reduced compared to control group （ P〈0.05 ） .Conclusions In

关 键 词：结肠炎 CAJAL间质细胞 c—kit 电子显微镜 大鼠 

分 类 号：R574.62[医药卫生—消化系统]