摘要
目的:观察脾气虚型变应性鼻炎大鼠鼻黏膜组织白细胞介素-2,4,6(IL-2,4,6,)mRNA的表达,探讨脾气虚与变应性鼻炎的病理相关性。方法以卵清蛋白法和卵清蛋白加饮食不节法分别建立大鼠变应性鼻炎模型(AR模型组)和脾气虚变应性鼻炎模型(脾虚AR模型组),分别取鼻黏膜组织,RT-PCR检测IL-2,4,6,mR-NA表达水平,进行组间比较。结果IL-2mRNA的表达空白组与模型组相比较具有显著性差异(P<0.05),模型组鼻黏膜组织IL-2mRNA的表达明显降低。IL-4mRNA的表达空白组与模型组相比较具有显著性差异(P<0.01、P<0.05),模型组鼻黏膜组织IL-4mRNA的表达明显升高,脾虚AR模型组升高更明显。IL-6mRNA的表达空白组与模型组相比较具有显著性差异(P<0.01、P<0.05),模型组鼻黏膜组织IL-6mRNA的表达明显升高,但AR模型组升高更明显。结论变应性鼻炎大鼠鼻黏膜组织IL-2表达明显降低,IL-4,6表达明显升高,脾虚AR模型组升高更明显。说明IL-2,IL-4,IL-6活性表达水平可能是脾虚型变应性鼻炎的一个重要因素。
Objective：Observed in rats with allergic rhinitis nasal mucosa of IL-2,4,6（IL-2,4,6,）mRNA expression to investigate spleen deficiency and pathological relevance of allergic rhinitis.Methods：To egg white protein ovalbumin method and improper diet method,respectively rat model of allergic rhinitis（AR model group）,and spleen deficiency model of allergic rhinitis（AR deficiency model group）,nasal mucosa were taken,RT-PCR detection of IL-2,4,6,mRNA expression levels were compared between groups.Results：The expression of IL-2mRNA control group compared with the model group with significant difference（P0.05）,model group,IL-2mRNA nasal mucosa was significantly reduced.The expression of IL-4mRNA control group compared with the model group with significant difference（P0.01,P0.05）,model group,the nasal tissue expression of IL-4mRNA significantly increased spleen AR model group increased more significantly.The expression of IL-6mRNA control group compared with the model group with significant difference（P0.01,P0.05）,model group,the nasal tissue expression of IL-6mRNA significantly increased,but the AR model group increased more significantly.Conclusion：Nasal mucosa of allergic rhinitis in rats significantly decreased the expression of IL-2,IL-4,6 expression was significantly increased in spleen was significantly increased in AR model group.Description IL-2,IL-4,IL-6 activity of spleen deficiency type expression may be an important factor in allergic rhinitis.
出处
《中华中医药学刊》
CAS
2010年第12期2486-2489,共4页
Chinese Archives of Traditional Chinese Medicine
