疏肝健脾方对实验性腹泻型肠易激综合征5-羟色胺相关的结肠黏膜离子通道转运机制的影响  

Effects of Shugan Jianpi Recipe on the Ion Transport of Diarrhea Predominant Irritable Bowel Syndrome Rat Colon Mucosa Induced by 5-HT

作　　者：张声生[1] 汪正芳[1] 郭前坤[1] 陈剑明[2] 李琳[2] 李萍[3] 

机构地区：[1]首都医科大学附属北京中医医院消化中心,北京100010 [2]北京中医药大学,北京100010 [3]北京市中医研究所,北京100010

出　　处：《中国中西医结合杂志》2012年第11期1516-1520,共5页Chinese Journal of Integrated Traditional and Western Medicine

基　　金：国家自然科学基金资助项目(No.30973746);北京市自然科学基金资助项目(No.7102083);北京市教委科技发展计划资助项目(No.KM201010025027)

摘　　要：目的探讨疏肝健脾方对实验性腹泻型肠易激综合征5-羟色胺(5-HT)相关的结肠黏膜离子转运的调节机制。方法将SD大鼠随机分成正常组、模型组、疏肝健脾组,每组12只;模型组及疏肝健脾组采用乙酸灌肠加束缚应激进行造模,造模成功后,正常组和模型组给予生理盐水,疏肝健脾组给予疏肝健脾方灌胃14天。在药物和特异性阻断剂的作用下,采用短路电流技术,体外测量5-HT引起的结肠上皮短路电流变化。结果 3组大鼠离体远端结肠基础电流、基础电压及跨膜电阻之间比较,差异无统计学意义(P>0.05)。5-HT引起的大鼠结肠黏膜产生的短路电流峰值模型组比正常组降低(P<0.05),疏肝健脾组较模型组升高(P<0.05)。在结肠黏膜的顶膜侧加入4,4'-diisothiocyanato-stilbene-2,2'-disulfonic acid(DIDS,500μmol/L)后,5-HT引起的短路电流峰值模型组比正常组降低(P<0.05),疏肝健脾组较模型组升高(P<0.05);当顶膜溶液中Na+被替换(无Na+)或顶膜侧加入阿米洛利(100μmol/L)后,5-HT引起的短路电流峰值模型组比正常组降低(P<0.05),疏肝健脾组较模型组升高(P<0.05)。结论疏肝健脾方对腹泻型肠易激综合征大鼠结肠黏膜5-HT通路相关的跨上皮电活动的作用是通过调节Cl-和HCO3-的分泌实现的,其调节是通过位于结肠上皮顶膜的囊性纤维化跨膜调控性Cl-通道,以及位于基底膜的Na+-K+泵、钠钾氯共转运体、钠碳酸氢根共转运体、Cl-/HCO3-交换器和基底膜K+通道共同作用的结果。Objective To investigate the mechanism of Shugan Jianpi Recipe （SJR） on the ion transportation of diarrhea predominant irritable bowel syndrome （IBS-D） colon mucosa induced by 5-HT. Methods Totally 36 male SD rats were randomly divided into three groups, i.e., the normal group, the model group, and the SJR group, 12 in each group. IBS-D Rat model was induced by intracolonic instillation of acetic acid and restraint stress. After successful modeling, normal saline was given to rats in the normal group and the model group, while SJR was given to those in the SJR group by gastrogavage for 14 days. The short circuit current （Isc） technology was used to measure 5-HT induced Isc changes of the colon mucosa under the actions of drugs and specific blocking agents. Results There was no difference in basal current （BC）, the potential difference （PD）, and transmembrane resistance （TR） of the distal colon among the 3 groups （all P0.05）. The 5-HT induced short circuit current change （△Isc） was lower in the model group than in the normal group （P0.05）, and it was higher in the SJR group than in the model group （P0.05）. When 4,4′-diisothiocyanato-stilbene-2,2′-disulfonic acid （DIDS, 500 μmol/L）, an Ca＋-dependent Cl-channel blocker, was added from the epiphragm of the colonic mucosa, the 5-HT induced △Isc was lower in the model group than in the normal group （P0.05）, and it was higher in the SJR group than in the model group （P0.05）. When Na＋ was substituted in the epiphragm solution （Na＋ free） or amiloride （100 μmol/L） was added from the epiphragm of the colonic mucosa, an epithelial Na＋ channel blocker, the 5-HT induced △Isc was lower in the model group than in the normal group （P0.05）, and it was higher in the SJR group than in the model group （P0.05）. Conclusions SJR could affect the transmembrane electrolyte transportation of IBS-D rat induced by 5-HT through regulating the secretion of Cl-and HCO3-. The effects might be achieved by the

关 键 词：疏肝健脾方 结肠上皮 腹泻型肠易激综合征 短路电流 

分 类 号：R285.5[医药卫生—中药学]