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脑源性神经营养因子在结肠炎后内脏高敏感小鼠中的调节作用
引用本文:杨静,于岩波,于卉,左秀丽,陈哲宇,李延青.脑源性神经营养因子在结肠炎后内脏高敏感小鼠中的调节作用[J].胃肠病学,2012,17(2):91-95.
作者姓名:杨静  于岩波  于卉  左秀丽  陈哲宇  李延青
作者单位:1. 山东省千佛山医院消化内科,250014;山东大学齐鲁医院消化内科
2. 山东大学齐鲁医院消化内科
3. 山东大学医学院神经生物学研究所
基金项目:本课题由国家自然科学基金
摘    要:背景:脑源性神经营养因子(BDNF)可调控突触可塑性和维持神经内环境的稳定,近年研究证实BDNF参与痛觉的调控。目的:研究BDNF在结肠炎后内脏高敏感小鼠中的调节作用。方法:以结肠内灌注三硝基苯磺酸(TNBS)诱导建立结肠炎后内脏高敏感模型。将小鼠分为BDNF+/+对照组、BDNF+/+TNBS炎症组、BDNF+/-对照组和BDNF+/-TNBS炎症组。行结肠和膀胱组织学检查,以ELISA法测定背根神经节内BDNF蛋白表达,记录各组对结直肠扩张的反应和膀胱敏感性。结果:TNBS对两种基因型小鼠均可诱导明显的结肠炎症。同一基因型小鼠TNBS炎症组背根神经节BDNF表达显著高于相应对照组(P〈0.05),同时伴有结肠和膀胱敏感性上调(P〈0.05)。BDNF+/-TNBS炎症组和对照组BDNF表达分别显著低于相应BDNF+/+小鼠(P〈0.05),BDNF+/-TNBS炎症小鼠的结肠和膀胱敏感性显著低于BDNF+/+TNBS炎症小鼠(P〈0.05)。除结直肠扩张压力≥60 mm Hg外,BDNF+/-对照小鼠的结肠和膀胱敏感性与BDNF+/+对照小鼠无明显差异。结论:BDNF对结肠炎后结肠高敏感和牵涉性膀胱高敏感具有调节作用。

关 键 词:脑源性神经营养因子  小鼠  基因敲除  结肠炎  内脏高敏感

Role of Brain-derived Neurotrophic Factor in the Modulation of Post-inflammatory Visceral Hypersensitivity in Mice
YANG Jing , YU Yanbo , YU Hui , ZUO Xiuli , CHEN Zheyu , LI Yanqing.Role of Brain-derived Neurotrophic Factor in the Modulation of Post-inflammatory Visceral Hypersensitivity in Mice[J].Chinese Journal of Gastroenterology,2012,17(2):91-95.
Authors:YANG Jing  YU Yanbo  YU Hui  ZUO Xiuli  CHEN Zheyu  LI Yanqing
Institution:1Department of Gastroenterology,Shandong Qianfoshan Hospital,Qianfoshan,Shandong Province(250014);2Department of Gastroenterology,Qilu Hospital,Shandong University,Jinan;3Department of Neurobiology,Shandong University School of Medicine,Jinan
Abstract:Background: Brain-derived neurotrophic factor(BDNF) can modulate the plasticity of synapses and maintain the environment of nervous system.Recent studies show that BDNF is also involved in pain modulation.Aims: To investigate the role of BDNF in the modulation of post-inflammatory visceral hypersensitivity in mice.Methods: Colitis model was induced in mice by enema with 2,4,6-trinitrobenzene sulfonic acid(TNBS).BDNF+/+ and BDNF+/- mice were divided into BDNF+/+ control group,BDNF+/+ TNBS-colitis group,BDNF+/- control group and BDNF+/- TNBS-colitis group.Histology examination of colon and bladder was performed.Expression of BDNF in dorsal root ganglia was determined by ELISA.Visceral response to colorectal distension and bladder sensitivity were recorded.Results: Colitis was successfully induced by TNBS in both genotypes mice.Expression of BDNF in dorsal root ganglia was significantly higher in both TNBS-colitis groups than that in corresponding control groups(P<0.05),and sensitivity of colon and bladder was up-regulated(P<0.05).Expression of BDNF in BDNF+/- TNBS-colitis group and BDNF+/- control group was significantly lower than that in BDNF+/+ TNBS-colitis group and BDNF+/+ control group,respectively(P<0.05).Sensitivity of colon and bladder in BDNF+/- TNBS-colitis group was significantly lower than that in BDNF+/+ TNBS-colitis group(P<0.05),while no significant difference was found between BDNF+/- control group and BDNF+/+ control group except with colorectal distention ≥ 60 mm Hg.Conclusions: BDNF participates in the modulation of post-inflammatory colonic and referred bladder hypersensitivity.
Keywords:Brain-Derived Neurotrophic Factor  Mice  Knockout  Colitis  Visceral Hypersensitivity
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