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目的观察哮喘大鼠肺组织中Toll样受体3(TLR3)和TLR9的表达及对布地奈德的影响,探讨TLRs在哮喘炎症机制中的作用。方法建立大鼠哮喘模型,随机分成哮喘组、对照组和布地奈德组,免疫组织化学法检测肺组织TLR3和TLR9的表达。结果哮喘组(OD值:0.201±0.034)和布地奈德组(OD值:0.195±0.043)肺组织TLR3的光密度值显著高于对照组(OD值:0.144±0.039)(P<0.05),布地奈德组与哮喘组差异无统计学意义。哮喘组(OD值:0.236±0.022)和布地奈德组(OD值:0.231±0.023)肺组织TLR9的光密度值均显著低于对照组(OD值:0.271±0.025)(P<0.05);布地奈德组与哮喘组差异无统计学意义;肺组织TLR3和TLR9蛋白的表达水平无显著相关性(n=26,r=-0.153)。结论哮喘大鼠肺组织TLR3蛋白表达升高,TLR9蛋白的表达则反之,TLRs的表达过度或不足可能是哮喘气道炎症的重要原因之一。布地奈德的抗炎作用可能主要不是通过TLR3和TLR9的途径实现。
Objective To observe the expression of TLR3 and TLR9 in lung tissue and the effect on the expression of budesonide in asthmatic rats and the role of TLRs in the mechanism of asthma inflammation. Methods The rat asthma model was established and randomly divided into asthma group, control group and budesonide group. Immunohistochemistry was used to detect the expression of TLR3 and TLR9 in lung tissue. Results The optical density of TLR3 in asthmatic group (OD: 0.201 ± 0.034) and budesonide group (OD: 0.195 ± 0.043) was significantly higher than that in control group (OD: 0.144 ± 0.039, P <0.05) There was no significant difference between budesonide group and asthma group. The OD value of TLR9 in asthma group (OD: 0.236 ± 0.022) and budesonide group (OD: 0.231 ± 0.023) were significantly lower than those in control group (OD: 0.271 ± 0.025) (P <0.05); There was no significant difference between budesonide group and asthma group. There was no significant correlation between TLR3 and TLR9 expression in lung tissue (n = 26, r = -0.153). Conclusion The expression of TLR3 protein in lung tissue of asthmatic rats is increased, whereas the expression of TLR9 protein is contrary. TLRs over- or under-expression may be one of the important causes of asthma airway inflammation. The anti-inflammatory effect of budesonide may not be achieved mainly through TLR3 and TLR9 pathways.