论文部分内容阅读
目的:观察鼻腔局部应用丙酸氟替卡松和左卡巴斯汀对实验性变应性鼻炎(AR)大鼠水通道蛋白5(AQP5)表达的影响。方法:40只Wister大鼠随机分为AR组30只和对照组10只。AR组建模后,随机均分为3组:AR+丙酸氟替卡松组(F组)、AR+左卡巴斯汀组(L组)和AR组(10只)。3组大鼠治疗28 d后,应用免疫组织化学检测AQP5在各组中的表达。结果:免疫组织化学显示AQP5在各组分布相同,统计学分析显示F组与AR组、L组比较,差异有统计学意义(P<0.05),但L组与AR组比较,差异无统计学意义(P>0.05);L组与对照组比较,差异有统计学意义(P<0.05)。结论:AQP5在实验性AR大鼠鼻黏膜的强表达,提示AQP5参与了AR的发病过程,与腺体过度分泌、组织水肿有关。糖皮质激素可以明显下调AQP5的表达量,H1受体阻滞剂对AQP5的表达量无明显影响。
Objective: To observe the effect of topical nasal administration of fluticasone propionate and levocabastine on aquaporin 5 (AQP5) expression in experimental allergic rhinitis (AR) rats. Methods: Forty Wister rats were randomly divided into AR group (n = 30) and control group (n = 10). AR models were randomly divided into three groups: AR + fluticasone propionate group (F group), AR + levocabastine group (L group) and AR group (10). After 28 days of treatment, the expression of AQP5 in each group was detected by immunohistochemistry. Results: Immunohistochemistry showed that the distribution of AQP5 in each group was the same. Statistical analysis showed that the difference between F group and AR group and L group was statistically significant (P <0.05), but there was no significant difference between L group and AR group (P> 0.05). There was significant difference between L group and control group (P <0.05). Conclusion: The strong expression of AQP5 in the nasal mucosa of experimental AR rats suggests that AQP5 is involved in the pathogenesis of AR, which is associated with hypersecretion of glands and tissue edema. Glucocorticoid can significantly reduce the expression of AQP5, H1 receptor blockers on the expression of AQP5 no significant effect.