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作 者:杨成[1] 张声生[1] 李晓玲[1,2] 汪正芳[1]
机构地区:[1]首都医科大学附属北京中医医院,北京100010 [2]北京中医药大学,北京100029
出 处:《中华中医药杂志》2015年第12期4268-4271,共4页China Journal of Traditional Chinese Medicine and Pharmacy
基 金:国家自然科学基金(No.81473644);北京市医院管理局临床医学发展专项经费资助项目(No.ZY201411);北京市卫生系统高层次卫生技术人才培养计划(No.2011-2-13)~~
摘 要:目的:观察痛泻要方对内脏高敏感大鼠的影响,初步探讨其作用机制。方法:30只SD幼鼠随机分为正常组、模型组和中药组。采用母婴分离联合束缚应激的方法建立腹泻型肠易激综合征(IBS-D)大鼠内脏高敏感模型。正常组、模型组予0.9%氯化钠溶液,中药组予痛泻要方煎剂灌胃。给药前后,观察3组大鼠粪便Bristol分级评分、粪便含水量及腹壁撤退反射(AWR);采用Real-Time PCR法检测结肠CFTR Cl-通道蛋白表达。结果:模型组粪便Bristol评分、含水量均高于正常组,内脏痛阈值下降(P<0.01);给药后,中药组Bristol评分及含水量下降(P<0.01),内脏疼痛阈值升高(P<0.01);与正常组及模型组比较,中药组结肠CFTR Cl-通道蛋白表达水平下降(P<0.05)。结论:痛泻要方可以降低IBS-D大鼠内脏敏感性,机制可能是通过影响结肠上皮的CFTR Cl-通道蛋白表达。Objective: To observe effects of Tongxie Yaofang Formula(TXYF-Formula) on visceral hypersensitivity rats, and explore its mechanism. Methods: 30 SD rats were randomly divided into normal group, model group and traditional Chinese medicine(TCM) group. The diarrhea-predominant irritable bowel syndrome(IBS-D) rat models with visceral hypersensitivity were established by suing method of combination of maternal separation and restraint stress. Rats in normal and model groups received gavage administration with normal saline and rats in TCM group received gavage administration with TXYF-Formula. Scores of Bristol classii cation and water content of the fecal pellets and abdominal withdrawal rel ex(AWR) of rats in all the groups were observed before and after treatment. The expression of CFTR Cl-channel protein in colon was detected by using RTPCR method. Results: Compared with normal group, stool Bristol score and water content of rats in model group was higher, and the visceral pain threshold was lower(P〈0.01). After treatment, Bristol score and water content of rats in TCM group was declined(P〈0.01), and the visceral pain threshold was increased(P〈0.01). Compared with normal and model groups, the expression of CFTR Cl-channel protein in colon of rats in TCM group was decreased(P〈0.05). Conclusion: TXYF-Formula could reduce the visceral sensitivity of IBS-D rats, and the mechanism might be related with its inl uence on expression of CFTR Cl-channel protein in colon.
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