鼻敏感颗粒对变应性鼻炎小鼠炎症反应及相关蛋白表达的影响

Study on the Effects of Nasal Sensitive Particles on Inflammatory Response and the Expression of Related Proteins of AR Mice

目的观察鼻敏感颗粒对变应性鼻炎(AR)小鼠炎症反应的影响并探讨其机制。方法小鼠随机分成模型组、正常组、阳性对照组、鼻敏感颗粒低剂量组、鼻敏感颗粒中剂量组和鼻敏感颗粒高剂量组,除正常组外,其他各组小鼠制备AR模型,阳性对照组灌胃氯雷他定药液,鼻敏感颗粒低、中、高剂量组分别灌胃相应剂量鼻敏感颗粒药液。观察各组小鼠鼻部症状评分、鼻腔病理形态与病变评分,检测血清炎性因子含量,鼻黏膜GATA3、T-bet蛋白和mRNA相对表达量。结果给药7、14、28 d模型组小鼠症状评分较正常组显著升高,给药7、14、28 d阳性对照组、鼻敏感颗粒低、中、高剂量组小鼠症状评分较模型组显著降低,差异有统计学意义(P<0.05);和正常组相比,模型组小鼠鼻黏膜组织GATA3蛋白表达升高,T-bet蛋白表达降低;和模型组相比,阳性对照组、鼻敏感颗粒低、中、高剂量组小鼠鼻黏膜组织GATA3蛋白表达降低,T-bet蛋白表达升高,差异有统计学意义(P<0.05)。结论鼻敏感颗粒可显著缓解AR小鼠临床症状,降低血清炎性因子含量,其机制可能和改善Th1/Th2细胞失衡有关。

Objective:To analyze the effects of Nasal Sensitive Particles on the inflammatory response and the mechanism on allergic rhinitis(AR)mice. Methods:The mice were randomly divided into the model group,the normal group,the positive control group,low-dose group,middle dose group and high dose group. Except the normal group,the other groups were prepared for AR model. The control group was intragastrically administered with loratadine solution,and Nasal Sensitive Particles groups were intragastrically administered with different doses. The nasal symptom scores,nasal pathological morphology and lesion scores,serum inflammatory factor content and the relative expression of GATA3,T-bet protein and mRNA in nasal mucosa were observed. Results:The symptom scores in the model group on 7 th,14 th,and 28 th days were significantly higher than those in the normal group.Those of Nasal Sensitive Particles groups were significantly lower than those in the model group. The difference was statistically significant(P < 0.05). Compared with the normal group,the expression of GATA3 protein of the model group was increased,and the expression of T-bet protein was decreased. Compared with the model group,the expression of GATA3 protein in Nasal Sensitive Particles groups decreased,and the expression of T-bet protein increased;the difference was statistically significant(P < 0.05). Conclusion:Nasal Sensitive Particles can significantly alleviate the clinical symptoms of AR mice and reduce the serum inflammatory factor content. The therapeutic mechanism may be related to the improvement of Th1/Th2 cell imbalance.