AQP1在慢传输型便秘发病过程中的作用机制探讨

目的:通过建立大鼠慢传输型便秘模型,探讨AQP1在慢传输型便秘发病过程的作用机制。方法:SD大鼠48只,随机分为4组:空白组,模型组,莫沙必利治疗组,麻仁丸治疗组。空白组大鼠用生理盐水灌胃,便秘模型组和治疗组大鼠分别用复方地芬诺酯灌胃,建立大鼠慢传输型便秘模型。模型建立后,治疗组大鼠分别用莫沙必利、麻仁丸灌胃,观察各组大鼠大便粒数及大便湿重。治疗结束后将大鼠集体处死,取大鼠近端结肠标本,用免疫组织化学的方法检测各组大鼠近端结肠AQP1的表达情况。采用彩色病理图像分析系统对阳性表达的平均光密度值进行半定量分析。结果:便秘组结肠AQP1的平均光密度(MD)值大于空白对照组、莫沙必利治疗组、麻仁丸治疗组的MD值(P<0.05),差异有统计学意义;莫沙必利治疗组和麻仁丸治疗组的MD值均大于空白对照组(P<0.05),差异有统计学意义。结论:大鼠近端结肠AQP1的表达增高使结肠对水分的吸收增加,从而引起大便干结,排便困难,导致慢传输便秘的发生。

Study on the role of AQP1 in the pathogenesis of slow transit constipation

Objective： Establish the rat model of slow transit constipation（ STC） in order to research the role of AQP1 in the pathogenesis of slow transit constipation. Methods： 48 SD rats were randomly divided into 4 groups： blank group,model group,mosapride group and Maren pill group. The rats of blank group were given normal saline by gastric irrigation,while the rats of model group and treatment groups were given Diphenoxylate by intragastric administration before treated. When the model of STC is established,the rats of treatment groups were respectively given mosapride and Maren Pills. To observe the stool grain and stool wet weight. Finally killed all the rats and collected the proximal colons. Detect expression of AQP1 in the proximal colon by immunohistochemistry. The positive average optical densities were analyzed semiquantitatively by computerized color image analyzer. Results： The density means（ MD） of AQP1 in the colon of model group were greater than the blank control group,mosapride group and Maren pill group（ P 〈 0. 05）. The difference was statistically significant; The density means（ MD） of mosapride group and Maren Pill group were higher than blank control group（ P 〈 0. 05）. The difference was statistically significant. Conclusion： The increased expression of AQP1 in proximal colon of rats may lead to absorbing much more moisture,thus make stool dry and defecate difficult. It caused the occurrence of slow transit constipation.