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Effect of TongXie-YaoFang on Cl(−) and HCO(3) (−) Transport in Diarrhea-Predominant Irritable Bowel Syndrome Rats

TongXie-YaoFang (TXYF) can effectively alleviate the symptoms of diarrhea-predominant irritable bowel syndrome (D-IBS) patients. However, the curative mechanism has not been fully clarified. The study was designed to investigate the effect of TXYF on the colonic ion transport induced by serotonin (5...

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Detalles Bibliográficos
Autores principales: Lu, Xiaofang, Zhang, Shengsheng, Yang, Cheng, Wang, Zhengfang, Zhao, Luqing, Wu, Zhenyu, Xie, Jing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4923577/
https://www.ncbi.nlm.nih.gov/pubmed/27403199
http://dx.doi.org/10.1155/2016/7954982
Descripción
Sumario:TongXie-YaoFang (TXYF) can effectively alleviate the symptoms of diarrhea-predominant irritable bowel syndrome (D-IBS) patients. However, the curative mechanism has not been fully clarified. The study was designed to investigate the effect of TXYF on the colonic ion transport induced by serotonin (5-HT) in D-IBS rats. A method of multiple stress (neonatal maternal separation (NMS) combined with restraint stress (RS)) was used to induce the D-IBS model. The model rats were randomly divided into two groups: NMS + RS group and TXYF-formula group, and the normal control (no handling) rats were classified as NH group. In the NMS + RS group, the change of short-circuit current (ΔI (sc)) induced by 5-HT was lower than that in the NH and TXYF-formula groups. After removing of the extracellular Cl(−) or HCO(3) (−) or basolateral Na(+) or blocking the cystic fibrosis transmembrane conductance regulator (CFTR), Na(+)-K(+)-2Cl(−) cotransporter (NKCC), Na(+)-HCO(3) (−) cotransporter, Cl(−)/HCO(3) (−) exchanger, K(+) channel, or Na(+)/K(+)-ATPase, respectively, there was no difference in 5-HT-induced ΔI (sc) among the three groups. These data suggest that TXYF can regulate 5-HT-induced Cl(−) and HCO(3) (−) secretion, possibly mediated by the combined action of CFTR, NKCC, Na(+)-HCO(3) (−) cotransporter, Cl(−)/HCO(3) (−) exchanger, K(+) channel, and Na(+)/K(+)-ATPase.