摘要
目的观察移动抑制因子(MIF)在实验性结肠炎的肠壁神经组织中的表达,探讨肠神经系统对结肠炎中MIF活性的调控作用。方法以半抗原二硝基氯苯(DNCB)给经过致敏的大鼠和小鼠灌肠诱发结肠炎,用二苯基四氮唑溴盐(MTT)法测定肠系膜淋巴细胞中MIF活性、用免疫荧光双染方法测定肠神经元中MIF蛋白的表达,观察ip6-羟基多巴(6-OHDA)和体外去甲肾上腺素(NE)培养对结肠炎时MIF活性的影响。结果结肠炎大鼠肠壁神经元MIF蛋白的表达随DNCB灌肠剂量的增大而增强;6-OHDA(38～150mg·kg-1体重)能够进一步刺激结肠炎小鼠MIF活性的升高(ip6-OHDA组与ip溶剂的结肠炎组相比,P<0.01);NE(1.0nmol·L-1～1.0mmol·L-1)体外可使结肠炎组的MIF活性升高,其反应幅度和敏感性大于对照组(两组相比,P<0.01)。结论DNCB引起的实验性结肠炎中MIF活性升高;正常的交感活动能够抑制结肠炎时的MIF活性。
Aim To observe the expression of migration inhibitory factor （MIF） in the enteric neurons, and to explore the nervous regulation on MIF activity in experimental colitis. Methods Colitis was induced in sensitized rat and mouse by 2, 4-dinitrochlorobenzene （DNCB） enema. MIF activity was measured both in the mesentery lymphocyte（ by MTT）and in the enteric neurons（ by immunofluorescence double staining）. 6-OHDA was intraperitonealy （ip） administered to mouse before DNCB treatment. Norepinephrine （ NE ） was added to lymphocyte culture in vitro during MIF preparation. Resuits The expression of MIF protein in enteric neuron was increased in DNCB-induced colitis in rat. ip 6-OH-DA in colitis mouse（38 - 150 mg · kg^-1） resulted in a further increase of MIF activity than ip vehicle in colitis mouse （P 〈0. 01 as 6-OHDA group vs vehicle group）. NE （ 1.0 nmol· L^-1 - 1.0 mmol · L^-1 ） could dose-dependently increase the MIF activity in vitro（ P 〈0. 01 vs zero point, respectively ）. The response amplitude and sensitivity to NE were higher in colitis group than in the control group （ P 〈 0. 01 vs control ）. Conclusion The MIF activity and MIF protein were increased in the experimental colitis induced by DNCB. The sympathetic nerve could inhibit the MIF activity in the colitis.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2007年第5期577-581,共5页
Chinese Pharmacological Bulletin
基金
国家自然科学基金资助项目(No30170419)
北京市自然科学基金资助项目(No7063083)
关键词
结肠炎
肠神经系统
移动抑制因子
二硝基氯苯
大鼠
小鼠
colitis
enteric nervous system
migration inhibitory factor
dinitrochlorobenzene
rat
mouse
