1. 南京中医药大学2014级硕士研究生,江苏,南京,210029
2. 江苏省中医院肛肠科,江苏,南京,210029
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郭海霞, 钱海华, 张丹, 等. 慢性传输型便秘“肠病及肺”相关机制实验研究[J]. 上海中医药杂志, 2017,51(7):15-19.
GUO Hai-xia, QIAN Hai-hua, ZHANG Dan, et al. Experimental study on related mechanism of “intestinal diseases affecting lung”in slow transit constipation[J]. Shanghai Journal of Traditional Chinese Medicine, 2017,51(7):15-19.
郭海霞, 钱海华, 张丹, 等. 慢性传输型便秘“肠病及肺”相关机制实验研究[J]. 上海中医药杂志, 2017,51(7):15-19. DOI:
GUO Hai-xia, QIAN Hai-hua, ZHANG Dan, et al. Experimental study on related mechanism of “intestinal diseases affecting lung”in slow transit constipation[J]. Shanghai Journal of Traditional Chinese Medicine, 2017,51(7):15-19. DOI:
目的:采用复方苯已哌啶建立慢性传输型便秘模型,通过观察肺、肠组织病理改变及水通道蛋白含量变化情况,初步阐明“肠病及肺”及从肺论治慢性传输型便秘的相关生物学基础。 方法:将20只SD大鼠随机分为正常组和模型组,每组10只,雌雄各半;正常组给予普通饲料喂养,模型组给予混有复方苯乙哌啶的饲料,造模时间为120天。造模结束后,测定大鼠24 h粪便量、含水量及小肠炭末推进率,观察结肠留存粪便粒数;采用HE染色技术观察大鼠肺、肠组织病理结构变化情况,采用免疫组化技术检测大鼠肺组织AQP1及肠组织AQP3含量变化。 结果:模型组大鼠排便量、粪便含水量、小肠炭末推进率及结肠存留粪便量较正常组均明显降低(P<0.01)。模型组大鼠肺、肠组织均出现不同程度的病理改变,肺组织中AQP1及结肠组织中AQP3在着色量及着色程度上均高于正常组(P<0.01)。 结论:采用复方苯乙哌啶成功复制出慢性传输型便秘模型,模型大鼠肺、肠组织均出现病理改变;肺组织AQP1及肠组织AQP3含量升高致津液代谢失常,可能是便秘“肠病及肺”及从肺论治慢性传输型便秘的生物学基础。
Objective:To preliminarily explore the related biological basis of the theory of “intestinal diseases affecting lung”and treatment from lung in slow transit constipation(STC)by the changes of the lung and intestine pathology and the content of aquaporins(AQPs)based on compound diphenoxylate induced STC model. Methods20 SD rats were randomly divided into the normal group and model group,10 rats in each group with male and female in half. The normal group was fed with normal diet,and the model group was fed with diet containing compound diphenoxylate,with a course of 120 days. After modeling,the fecal amount within 24 hours,the water content in faeces and the rate of carbon propelling in small intestine of rats were measured,and the number of retained fecal particles in colon was observed. The pathological changes of lung and intestine were observed by HE staining. The expression levels of AQP1 in lung and AQP3 in intestinal tissue were determined by immunohistochemistry. Results:Compared with the normal group,the fecal amount within 24 hours,the water content in faeces,the rate of carbon propelling in small intestine and the number of retained fecal particles in colon were significantly decreased in the model group(P<0.01). The pathological changes of lung and intestine with different degrees in rats were found in the model group. The coloring amount and degree of AQP1 in lung and AQP3 in colon in the model group were higher than those in the normal group(P<0.01). Conclusion:The model of slow transit constipation is successfully replicated by compound diphenoxylate. The obvious pathological changes of lung and intestine are observed in the model rats,and the increasing contents of AQP1 in lung and AQP3 in intestine induce the disorder of body fluid metabolism,which may be the biological basis of the theory of “intestinal diseases affecting lung”and treatment from lung in slow transit constipation
慢性传输型便秘肠病及肺从肺论治大鼠病理变化水通道蛋白
slow transit constipationintestinal diseases affecting lungtreatment based on lungratspathological changesaquaporin
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