脑源性神经营养因子在乳鼠结肠扩张刺激诱导的慢性内脏高敏感和肠道动力异常中的作用  

Role of Brain-derived Neurotrophic Factor in Alterations of Visceral Sensitivity and Intestinal Motility Induced by Neonatal Colon Irritation in Rats

作　　者：赖华梅[1] 诸琦[1] 王静[1] 张明均[1] 

机构地区：[1]上海交通大学医学院附属瑞金医院消化内科,200025

出　　处：《胃肠病学》2008年第4期223-227,共5页Chinese Journal of Gastroenterology

摘　　要：背景:慢性内脏高敏感和肠道动力异常是肠易激综合征(IBS)的主要病理生理特征,但两者的形成机制至今尚未明确。目的:研究乳鼠结肠扩张刺激动物模型成年后内脏感觉和肠道动力的变化以及脑源性神经营养因子(BDNF)在其中所起的作用,从而探讨BDNF在IBS发病机制中的作用。方法:建立乳鼠结肠扩张动物模型,通过检测成年大鼠对结直肠扩张的行为学反应评估内脏感觉,通过检测全胃肠和小肠传输功能评估肠道动力。比较腹腔注射BDNF抗体后内脏感觉和肠道动力的变化情况。以逆转录聚合酶链反应(RT-PCR)、蛋白质印迹法、酶联免疫吸附测定(ELISA)检测各组回肠、结肠BDNF及其受体TrkB的表达。结果:模型组成年后内脏敏感性增高,肠道动力增强。应用BDNF抗体后模型组内脏敏感性降低,肠道动力减弱。除成年期模型组结肠TrkBmRNA表达外,其余各组BDNF和TrkB mRNA表达均显著高于对照组(P<0.05)。乳鼠期和成年期模型组回肠、结肠BDNF和TrkB蛋白表达均显著高于对照组(P<0.05)。结论:BDNF在慢性内脏高敏感和肠道动力的变化中起一定作用,参与了IBS的发生。Background： Although visceral hypersensitivity and intestinal dysmotility are two main pathophysiologie features of irritable bowel syndrome （IBS）, the mechanisms of their development still remain uncertain. Aims： To study the alterations of visceral sensitivity and intestinal motility induced by neonatal colon irritation in rats and the role of brainderived neurotrophie factor （BDNF） in its development, and to explore the role of BDNF in the pathogenesis of IBS. Methods： A rat model was established by neonatal colon irritation. Visceral sensitivity was investigated by observing behavior response to colon irritation at 8th week. Intestinal motility was assessed by testing total gastrointestinal transit time at 10th week and small intestinal transit time at 11th week. The alterations of visceral sensitivity and intestinal motility were compared befor and after intraperitoneal injection of BDNF antibody. Expressions of ileal and colonic BDNF and its receptor TrkB were determined at 2nd and 1 lth week by reverse transeriptase polymerase chain reaction （RT-PCR）, Western blot and enzyme-linked immunosorbent assay （ELISA）. Results： Neonatal colon irritation resulted in visceral hypersensitivity and intestinal hypermotility in adult rats while BDNF antibodies attenuated visceral hypersensitivity and intestinal hypermotility. Compared with controls, the mRNA expression of ileal and colonic BDNF and TrkB were increased at 2nd and llth week except colonic TrkB mRNA expression at llth week （P〈0.05）, whereas the protein expression of ileal and colonic BDNF and TrkB were increased at 2nd and llth week in model group （P〈0.05）. Conclusions： BDNF may play a role in alterations of visceral hypersensitivity and intestinal dysmotility, and may be involved in the pathogenesis of IBS.

关 键 词：脑源性神经营养因子 内脏高敏感性 胃肠活动 肠易激综合征 

分 类 号：R574[医药卫生—消化系统]