食积因素对昆明小鼠血清IgA及肺脏与结肠组织SIgA、SP、VIP含量的影响

Influence of dyspepsia on the content of serum IgA and SIgA, SP, VIP in lung and colon tissue in the Kunming mice

目的:通过检测正常对照组与食积模型组小鼠血清IgA及肺脏、结肠组织分泌型免疫球蛋白A(SIgA)/P物质(SP)/血管活性肠肽(VIP)的含量,并分组进行相关性分析,探索"食积"的病理基础及"食积致病"的神经-内分泌-免疫调节机制。方法:采用自制高热量、高蛋白饲料喂养结合52%牛奶溶液灌服的方法,制作食积动物模型,检测血清IgA及肺脏、结肠组织中SIgA、SP、VIP的含量。结果:与正常对照组相比,食积模型组小鼠血清IgA、肺脏SP及VIP的含量降低(P<0.05),肺脏、结肠组织SIgA及结肠组织中SP含量呈现下调趋势,结肠组织中VIP呈现上调趋势,但差异无统计学意义。在正常对照组中,肺脏及结肠SIgA、SP、VIP各指标之间呈正性相关(P<0.05),血清IgA与肺脏SIgA、SP、VIP及结肠VIP之间呈负性相关(P<0.05);在食积模型组中,肺脏SIgA、SP、VIP各指标之间,血清IgA与结肠SIgA之间、结肠SP与SIgA、VIP之间呈正性相关(P<0.05)。结论:神经-内分泌-免疫调节紊乱可能是"食积"的病理基础及"食积致病"的病理机制。

Objective： in this study, the authors tried to detect the underlying pathology of suffering dyspepsia and the neuroendocrine immunomodulation mechanism dyspepsia might lead to by detecting the levels of serum IgA and SIgA/SP/VIP in lung and colon tissue aswellasthecorrelationanalysis. Methods： High protein and calorie diet induced mice model were built. The levels of IgA in serum and SIgA, SP, VIP in lung and colon tissue between the dyspeptic mice and the normal control mice had been compared. Results： Levels of serum IgA and VIP, SP in lung tissue were significantly lower in the dyspeptic mice than the normal control mice（P〈0.05）, and the levels of SIgA in lung and colon tissue, SP in colon tissue were lower in the dyspeptic mice, but there was not significant difference, while VIP in colon tissue were higher in the dyspeptic mice, while there was not significant difference. In the normal control mice, the correlation among SIgA, SP, VIP in lung/colon tissue was positive（P〈0.05）, while the correlation was negative between IgA in serum and SIgA, SP, VIP in lung tissue and VIP in colon tissue（P〈0.05）. In the dyspeptic mice, the correlation was positive among SIgA, SP, VIP in lung tissue, between IgA in serum and SIgA in colon tissue, SP and SIgA, VIP in colon tissue（P〈0.05）. Conclusion： Disorder of neuroendocrine immunomodulation may be the basic pathology of dyspepsia which may lead to relative diseases.