目的:观测慢性胃炎肝郁模型大鼠下丘脑和胃窦组织的P物质(SP)和胃动素(MLT)的表达,探讨肝郁型慢性胃炎的发病机制。方法:采用复合法(氨水加夜间束缚、断食、冰水游泳等)复制肝郁型慢性胃炎大鼠模型(病证组),设正常组、胃炎组、肝郁组予以对照。采用免疫组化法观察SP、MLT在下丘脑、胃窦组织的表达情况。结果:病证组大鼠下丘脑、胃窦组织中的SP、MLT的阳性产物的表达均降低,与胃炎组及非胃炎组(正常组、肝郁组)均有显著性差异(P<0.05)。结论:SP、MLT的释放不足可能是造成肝郁型慢性胃炎发病的神经生物学基础,也提示SP、MLT可作为评价慢性胃炎肝郁模型的参考指标。

Objective:To observe substance P(SP) and motilin(MLT) expression in hypothalamus and gastric antrum of rats with liver-qi stagnation syndrome of chronic gastritis,and to explore the mechanism of liver-qi stagnation syndrome of chronic gastritis. Methods:Rats were given ammonia,bounded at night,fasting and swam in cold water to establish the model of liver-qi stagnation syndrome of chronic gastritis. All rats were randomly divided into normal group,gastritis group,liver-qi stagnation syndrome group and liver-qi stagnation syndrome of chronic gastritis group. The expression of SP and MLT in hypothalamus and gastric antrum were observed by immunohistochemical method. Result:Compared with the normal group,gastritis group and liver-qi stagnation syndrome group,the expression levels of SP and MLT in hypothalamus and gastric antrum of liver-qi stagnation syndrome of chronic gastritis group were lower(P<0.05). Conclusion:The possible neurobiological mechanism of liver-qi stagnation syndrome of chronic gastritis is due to the changes of SP and MLT. SP and MLT could be regarded as indexes to evaluate the model of liver-qi stagnation syndrome of chronic gastritis.