摘要
目的:观察哮喘大鼠肺组织中Toll样受体4(TLR4)和5(TLR5)的表达及甲泼尼龙对该受体的影响,探讨TLRs在哮喘炎症机制中的作用。方法:建立哮喘大鼠模型,随机分成哮喘组、对照组和甲泼尼龙组,每组各9只,免疫组化法检测大鼠肺组织TLR4和TLR5的表达。结果:大鼠肺组织TLR4的光密度值哮喘组为(0.196±0.045),对照组为(0.172±0.025),两组比较差异无统计学意义(P>0.05);甲泼尼龙组为(0.142±0.019),显著低于对照组和哮喘组(P均<0.05)。肺组织TLR5的光密度值哮喘组为(0.185±0.029),显著高于对照组的(0.138±0.014)(P<0.05);甲泼尼龙组为(0.143±0.038),显著低于哮喘组(P<0.05),但与对照组比较差异无统计学意义(P>0.05)。肺组织TLR4和TLR5蛋白的表达水平无显著相关性(n=25,r=0.209)。结论:Ⅴ级鸡卵白蛋白致敏的哮喘大鼠肺组织TLR5蛋白的表达升高,TLR4无明显变化,TLR5在哮喘炎症中可能具有促炎作用。甲泼尼龙能下调TLR4和TLR5的表达,其抗炎机制可能与下调TLR4和TLR5水平有关。
Objective： To investigate the potential roles of toll-like receptor （TLR） in pathogenesis of asthma inflammation; the expression of TLR4 and 5 which affected by methylpreduisolone were determined in a rat asthma model. Methods： Rat models of asthma were randomly divided into three groups on average, including an asthma group, a control group and a methylprednisolone treatment group. The expression of TLR4 and TLR5 protein were detected by immunohistochemical method. Results： There was no significant difference of TLR4 protein expression between the asthma group （0. 196±0.045 optical density） and the control group （0. 172±0.025 optical density） （P〉0.05）. Whereas, in the methylprednisolone treatment group （0. 142±0. 019 optical density）, the expression of TLR4 was significantly lower than that in the control group and in the asthma group （ P〈0.05 ）. Dramatically, the expression of TLR5 at lung tissue in the asthma group （0. 185±0. 029 optical density） was significantly higher than that in the control group （0. 138±0. 014 optical density） （P〈0.05）. Moreover, in the methylprednisolone treatment group it （0. 143±0. 038 optical density） was strongly lower than that in the asthma group, while there was no significant difference of TLR5 protein expression between the methylprednisolone treatment group and the control group （ P〉0.05 ）. Furthermore, there was no significant correlation between levels of TLR4 and TLR5 at lung tissue （ n = 25, r = 0. 209 ）. Conclusions： The level of TLR5 in asthmatic rat lung tissue was elevated, whereas no changes of TLR4 expression were observed. The elevated TLR5 indicated that it may play as a stimulative inflammatory mediator in asthma exacerbation. Data also showed the expression of TLR4 and TLR5 can be down-regulated by methylprednisolone ; this anti-inflammation function of methylprednisolone may be via TLR4 and TLR5 pathway.
出处
《儿科药学杂志》
CAS
2014年第5期1-4,共4页
Journal of Pediatric Pharmacy
基金
温岭市科技局基金资助项目(2009-2-55)
