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作 者:陈思羽[1] 黄会云[1] 陈玉[2] 平倩[2] 张涛[1]
机构地区:[1]广西中医药大学附属瑞康医院消化内科,广西南宁530011 [2]广西中医药大学
出 处:《胃肠病学和肝病学杂志》2016年第1期43-46,共4页Chinese Journal of Gastroenterology and Hepatology
基 金:国家自然基金(81260536);广西自然基金(2013GNSFAA019116)
摘 要:目的通过检测溃疡性结肠炎(ulcerative colitis,UC)结肠黏膜组织形态学、超微结构变化及结肠黏膜扣带蛋白(cingulin)、claudin-2表达,探讨UC发病的可能机制。方法 40只清洁级雄性Balb-c小鼠随机分为2组,其中正常组10只,模型组30只。除正常组外,模型组采用自由应用DSS法制备UC模型,于第8周末处死全部小鼠。应用光镜及透射电镜观察结肠黏膜组织形态学、超微结构及上皮黏膜屏障变化;应用AB-PAS及HID-AB染色观察结肠黏蛋白变化;应用Real-time PCR技术检测结肠黏膜cingulin、claudin-2表达。结果模型组光镜下见结肠黏膜不同程度缺损、溃疡形成,表面可见坏死组织及隐窝脓肿形成;电镜下见肠上皮细胞表面微绒毛稀疏,细胞连接间隙增宽,杯状细胞减少,线粒体肿胀,结构不清或呈空泡样变,部分可见核固缩,并见凋亡小体。模型组结肠黏蛋白表达明显较正常组减少,差异有统计学意义(P<0.05)。模型组cingulin、claudin-2表达分别为2.32±0.47、2.41±0.65,与正常组比较,其表达呈下降趋势,差异有统计学意义(P<0.05)。结论 cingulin通过促进claudin-2表达上升,破坏肠黏膜屏障完整,增加肠黏膜通透性导致结肠黏膜免疫反应异常,可能在UC发病中占据重要地位。Objective To investigate the mechanism of ulcerative colitis (UC) via the observation of colon mucosa morphological and uhrastructural and the expressions of cingulin, claudin-2. Methods Forty Balb-c rats were randomly divided into normal group and model group. Except normal group, the model group was administrated by drinking 5% DSS for the preparation of UC model. All rats were sacarificed after eighth weeks. The mucosa tissue morphology, colon- ic uhrastructure and the epithelial mucosa barrier were detected by the light microscope and electron microscope respec- tively. The changes of colonic mucin were detected by AB-PAS and HID-AB staining. The expressions of cingulin and claudin-2 in the colonic mucosa were detected by Real-time PCR. Results There were different degrees of defected colon- ic mucosa, ulceration and crypt abscess with necrotic tissue on surface under light microscope in model group. Also there were microvilli sparse on the intestinal epithelial cell, the intercellular spaces, the decreased goblet cells, the swelling mitochondria, the unclear structure with vacuolar degeneration, the pyknosis nuclear and apoptotic bodies under electron microscope. The expressions of colonic mucin secretion in model group was significantly higher than taht in the normal group (P 〈 0.05 ). The expressions of cingulin and claudin-2 in model group were 1.03 ± 0.39 and 1.12 ±0.26 respectively and there was a statistical difference compared with normal group (P 〈0.05). Conclusion Cingulin plays an important role in the control of clan- din-2 expression and response to the onset of UC.
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