跨膜蛋白16A介导感染后肠易激综合征中白细胞介素-4对Cajal细胞损伤的机制  

Mechanism of transmem-brane protein 16A in the impairment of intestinal cell of Cajal induced by interleukin-4 in postinfectious irritable syndrome

作　　者：刘书中[1] 陈明锴[1] 郑双英[1] 沈世强[1] 罗和生[1] 

机构地区：[1]武汉大学人民医院消化疾病研究所,430060

出　　处：《中华实验外科杂志》2013年第5期958-960,共3页Chinese Journal of Experimental Surgery

基　　金：基金项目：国家自然科学基金资助项目（81170350）;湖北省自然科学基金资助项目（2009CDB283）

摘　　要：目的探讨感染后肠易激综合征（PI-IBS）中跨膜蛋白16A（TMEM16A）介导白细胞介素4（IL-4）在Cajal细胞（ICC）损伤中的作用及机制。方法将30只SD雄性大鼠随机分为模型组（n=15）及对照组（n=15）。模型组以2，4，6-三硝基苯磺酸（TNBS）溶液灌肠，对照组以等量生理盐水灌肠，4周后取材。分别运用酶联免疫吸附试验（ELISA）法、免疫荧光、逆转录-聚合酶链反应（RT—PCR）及透射电镜检测各组大鼠IL4、TMEM16A的表达分布与ICC超微结构的相关改变。结果模型组结肠黏膜IL-4浓度[（2821．32±131．27）pg／g]较对照组[（2443．02±104．45）pg／g]明显上升（P〈0．01）。TMEM16A在PI—IBS模型大鼠结肠中的分布密度及表达水平上均低于对照组。PI—IBS组中，ICC出现超微结构损伤，与周围细胞缝隙连接减少。结论IL-4可能通过影响TMEM16A的表达分布造成ICC结构功能损伤，进而导致PI—IBS中胃肠动力的改变。Objective To investigate the mechanism of transmem-brane protein 16A （TMEM16A） in impaired intestinal cell of Cajal （ICC） induced by interleukin-4 （IL-4） in postinfeetious irritable syndrome （PI-IBS）. Methods Thirty male SD rats were randomly divided into the model group （ n = 15 ） and the control group （ n = 15 ）. Rats in the model group were given 2, 46-trinitro-benzene-sulfonic acid （TNBS） to establish a PI-IBS model. Other rats in the control group were given the same amount of saline as control. Animals were sacrificed after 4 weeks, enzyme linked immunosorbent assay （ELISA） test, immunohistochemistry, reverse transcriptase-polymerase chain reaction （RT-PCR） and transmission electron microscopy （TEM） were applied to observe the expression of IL-4 and TMEM16A and the changes of ICC ultrastructure. Results The Elisa test showed that the concentration of colonic IL-4 in the model group was higher than that in the control group （P 〈 0. 01 ）. hnmunotluorescence and RT-PCR suggested that the distribution and expression of TMEM16A were relatively lower compared with the controls. The TEM revealed the injury of ICC ultrastructure and its decreasing connection with other cells. Conclusion IL-4 may induce the injury of ICC by influencing the distribution and expression of TMEM16A, it could change the gastrointestinal motility and finally result in the occurrence of PI-IBS.

关 键 词：感染后肠易激综合征 CAJAL细胞 跨膜蛋白16A 白细胞介素-4 胃肠动力 

分 类 号：R57[医药卫生—消化系统]