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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。
AIM: To investigate the expression of TLR4 and TLR5 in the lung tissue of asthmatic rats and the effect of methylprednisolone on TLR4 expression in asthmatic rats. Methods: The asthmatic rat model was established and randomly divided into asthma group, control group and methylprednisolone group, with 9 rats in each group. The expression of TLR4 and TLR5 in lung tissue of rats were detected by immunohistochemistry. Results: The optical density of TLR4 in lung tissue was (0.196 ± 0.045) in asthma group and (0.172 ± 0.025) in control group, there was no significant difference between the two groups (P> 0.05) ± 0.019), which were significantly lower than those in control group and asthma group (all P <0.05). The optical density value of TLR5 in lung tissue was (0.185 ± 0.029) in asthma group, which was significantly higher than that in control group (0.138 ± 0.014) (P <0.05), that of methylprednisolone group was (0.143 ± 0.038) P <0.05), but no significant difference compared with the control group (P> 0.05). Lung tissue TLR4 and TLR5 protein expression levels were not significantly correlated (n = 25, r = 0.209). Conclusion: The expression of TLR5 protein in the lung tissue of asthmatic rat sensitized with grade Ⅴ chickens increased. There was no significant change in TLR4. TLR5 may have a proinflammatory role in asthmatic inflammation. Methylprednisolone can down-regulate the expression of TLR4 and TLR5, and its anti-inflammatory mechanism may be related to the down-regulation of TLR4 and TLR5 levels.