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痛泻要方对腹泻型肠易激综合征大鼠Cl(-)和HCO3 (-)转运的影响

Effect of TongXie-YaoFang on Cl(-) and HCO3 (-) Transport in Diarrhea-Predominant Irritable Bowel Syndrome Rats.

作者信息

Lu Xiaofang, Zhang Shengsheng, Yang Cheng, Wang Zhengfang, Zhao Luqing, Wu Zhenyu, Xie Jing

机构信息

Digestive Disease Center, Beijing Hospital of Traditional Chinese Medicine Affiliated to Capital Medical University, Beijing 100010, China.

出版信息

Evid Based Complement Alternat Med. 2016;2016:7954982. doi: 10.1155/2016/7954982. Epub 2016 Jun 14.

Abstract

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 HCO3 (-) or basolateral Na(+) or blocking the cystic fibrosis transmembrane conductance regulator (CFTR), Na(+)-K(+)-2Cl(-) cotransporter (NKCC), Na(+)-HCO3 (-) cotransporter, Cl(-)/HCO3 (-) 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 HCO3 (-) secretion, possibly mediated by the combined action of CFTR, NKCC, Na(+)-HCO3 (-) cotransporter, Cl(-)/HCO3 (-) exchanger, K(+) channel, and Na(+)/K(+)-ATPase.

摘要

痛泻要方(TXYF)能有效缓解腹泻型肠易激综合征(D-IBS)患者的症状。然而,其治疗机制尚未完全阐明。本研究旨在探讨痛泻要方对D-IBS大鼠中5-羟色胺(5-HT)诱导的结肠离子转运的影响。采用多种应激方法(新生鼠母婴分离(NMS)联合束缚应激(RS))诱导D-IBS模型。将模型大鼠随机分为两组:NMS + RS组和痛泻要方组,正常对照(未处理)大鼠作为NH组。在NMS + RS组中,5-HT诱导的短路电流变化(ΔIsc)低于NH组和痛泻要方组。分别去除细胞外Cl(-)或HCO3 (-)或基底外侧Na(+)或阻断囊性纤维化跨膜传导调节因子(CFTR)、Na(+)-K(+)-2Cl(-)共转运体(NKCC)、Na(+)-HCO3 (-)共转运体、Cl(-)/HCO3 (-)交换体、K(+)通道或Na(+)/K(+)-ATP酶后,三组间5-HT诱导的ΔIsc无差异。这些数据表明,痛泻要方可能通过CFTR、NKCC、Na(+)-HCO3 (-)共转运体、Cl(-)/HCO3 (-)交换体、K(+)通道和Na(+)/K(+)-ATP酶的联合作用来调节5-HT诱导的Cl(-)和HCO3 (-)分泌。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e68/4923577/d900f5d949b1/ECAM2016-7954982.001.jpg

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