锌营养状态对哮喘小鼠气道组织IL-12、NF-κB表达的影响

Effects of zinc nutritional status on the expressions of IL-12 and NF-κB in airway tissues of asthmatic mice

目的:探讨不同锌含量饮食对哮喘小鼠气道组织IL-12,NF-κB表达的影响。方法:建立进食低锌、正常锌、高锌饲料的哮喘小鼠模型。48只BALB/c小鼠,随机分为6组,每组8只。A组为正常饲料喂养+生理盐水激发;B组为高锌饲料喂养+卵清蛋白(OVA)激发;C组为高锌饲料配对喂养+OVA激发;D组为正常饲料喂养+OVA激发;E组为正常饲料配对喂养+OVA激发;F组为低锌饲料喂养+OVA激发。利用免疫组化检测气道组织IL-12,NF-κB表达水平。结果:与A组比较,B组、C组、D组、E组和F组IL-12表达下调(P<0.05),NF-κB表达上调(P<0.05);F组较B组、C组、D组和E组IL-12表达下调(P<0.05),NF-κB表达上调(P<0.05);B组与D组比较,C组与E组比较,IL-12表达无明显差异(P>0.05),NF-κB表达下调(P<0.05);B组、D组与本身的配对组比较,IL-12和NF-κB的表达无明显变化。结论:锌摄入不足可导致哮喘小鼠气道炎症反应加重;锌摄入不足可加剧哮喘小鼠气道组织IL-12表达下调、NF-κB上调。

Objective To investigate the effects of dietary zinc status on the expressions of IL-12 and NF-κB in airway tissues of asthmatic mice.Methods Animal models of asthma and dietary zinc status were established,48 BALB / c mice,were randomly divided into 6 groups with 8 mice each group.Zinc normal diet with saline stimulated group(group A);High levels of zinc diet with ovalbumin(OVA) stimulated group(group B);High levels of zinc pair-fed diet with OVA stimulated group(group C);Zinc normal diet with OVA stimulated group(group D);Zinc normal pair-fed diet with OVA stimulated group(group E);Zinc deficient diet with OVA stimulated group(group F).The contents of IL-12 and NF-κB in airway tissues were detected with immunohistochemistry.Results Compared with group A,the expression of IL-12 of group B,C,D,E and F were decreased(P<0.05),but NF-κB were increased(P<0.05);Compared with group B,C,D and E,IL-12 expression of group F were reduced(P<0.05),but NF-κB were increased(P<0.05);There were no statistically differences(P>0.05) between group B and its own control group in IL-12 expression,but NF-κB were reduced(P<0.05),the same as group D,The differences of expressions of IL-12 and NF-κB between Group B and its pair-fed group were not statistical(P>0.05),the same as the group D.Conclusion Insufficiency of zinc intake may lead to increased airway inflammation;Insufficiency of zinc intake can aggravate the decrease of IL-12 generating and increase of NF-κB generating in airway tissues of mice models of asthma.