【作者】 张少军；

【导师】 易建华；

【作者基本信息】 华中科技大学 ， 内科学， 2010， 硕士

【摘要】 目的:建立肝性胃肠功能障碍大鼠模型,采用免疫组织化学方法观察和比较正常组和模型组大鼠胃肠道cajal间质细胞分布、形态及数量变化,探讨肝性胃肠功能障碍可能的发病机制。方法:(1)动物分组及处理:正常SPF级Wistar雌性大鼠65只,随机分为2组:肝性胃肠功能障碍模型组(简称模型组)35只,以硫代乙酰胺350mg/kg腹腔注射,每天1次,连续3次;正常对照组(简称正常组)30只,同时间点等量生理盐水腹腔注射。观察大鼠的临床表现并测定大鼠胃排空速率及全胃肠通过时间来判断造模是否成功。(2)取材和检测:取肝及胃肠道组织,常规病理切片HE染色观察正常组和模型组肝及胃肠道组织病理变化;免疫组化染色检测正常组和模型组胃肠道Cajal间质细胞并进行半定量分析。结果:(1)与正常组相比,模型组大鼠出现典型胃肠道症状及肝性脑病症状且全胃肠通过时间及胃排空速率明显延迟(P<0.05),确认为肝性胃肠功能障碍模型造模成功。(2)与正常组相比,模型组肝及胃肠道组织常规病理切片HE染色肝组织坏死及胃黏膜和肠壁损伤明显。(3)与正常组相比,模型组胃肠道c-kit阳性Cajal间质细胞数量显著减少(P<0.05)且形态发生改变。结论:(1)硫代乙酰胺(350mg/kg腹腔注射,每天1次连续3次)可以成功诱导肝性胃肠功能障碍大鼠模型。(2)大鼠肝性胃肠功能障碍可能与Cajal间质细胞数量减少及形态改变有关。更多还原

【Abstract】 Objective:To establish the models of gastrointestinal dysfunction of rats with acute hepatic failure, and explore its pathogenesis by examining and comparing the distribution and quantity of interstitial cells of cajal ( ICC ) in the gastrointestinal tract of normal and model rats by immunohistochemical study.Methods:(1) Dividing and building model: Sixty-five female wistar rats were randomly divided into normal control group and model group. The latter group included thirty-five cases of rat were intraperitoneally injected with thioacetamide (TAA, 350mg/kg), three times at same time for three days. The former group included thirty cases of rat were intraperitoneally injected with physiologic saline for substitute served as controls. Then we observed the clinical manifestations of rats. The models of gastrointestinal dysfunction of rats with acute hepatic failure were defined by the delay of gastric emptying velocity and trans-gastrointestinal time. (2) Collecting sample and testing: To observe condition of liver and gastrointestinal tract both in normal and model rats by HE staining. Immunohistochemical study was used to examine and compare the distribution and quantity of interstitial cells of cajal in the gastrointestinal tract of normal and model rats. Results:(1) When compared with the normal control group, typical performance of gastrointestinal dysfunction and hepatic encephalopathy occurred in the model group,trans-gastrointestinal time and gastric emptying velocity of the model group were significantly delayed ( P<0.05 ). The gastrointestinal dysfunction models of rats with acute hepatic failure were induced successfully. (2) Compared with the normal control group, the HE staining showed that necrosis of liver tissue and injury of gastrointestinal tract occurred in the model group. (3) Compared with the normal control group, the immunohistochemical staining showed in the model group that ICC were greatly reduced in the gastrointestinal tract ( P<0.05 ).Conclusion:(1) The models of gastrointestinal dysfunction of rats with acute hepatic failure can be induced by intraperitoneal injection with TAA ( 350mg/kg ), three times at same time for three days. (2) The quantity of ICC in the gastrointestinal tract is reduced. The loss of ICC may play a key role in the pathogenesis of gastrointestinal dysfunction in rats with acute hepatic failure.更多还原