中文摘要：

目的：研究银翘散对甲型流感病毒诱导的肺炎小鼠肺组织中TLR-7介导的MyD88依赖性信号传导通路的调控机制。方法：将48只昆明小鼠随机分为正常对照组、模型组、利巴韦林组,银翘散低、中、高剂量组（20、10、5 g·kg·d-1）。除正常组外,建立流感病毒FM1鼠肺适应株滴鼻感染的小鼠流感病毒性肺炎模型。感染后1 h,正常组和模型组予以双蒸水灌胃,药物组分别予以各药物治疗,连续3 d。以苏木素-伊红染色（HE染色）法观察病理改变;RT-PCR检测肺组织TLR-7、髓样分化因子88（MyD88）、核因子（NF-κB p65）mRNA水平。结果：银翘散20、10 g·kg·d-1均能减轻肺组织炎性损伤;降低了TLR-7、Myd88、NF-κB P65 mRNA水平（P〈0.05,P〈0.01）。结论：银翘散通过抑制TLR-7介导的MyD88依赖性信号通路,抑制了NF-κB p65的表达,从而达到减少肺组织损伤的治疗目的。

英文摘要：

Objective ： To investigate influence of the representative prescriptions of Yinqiao Powder on expression of inflammatory cytokines and TLR7 - MyD88 - NF - кB P65 protein on influenza viral pneumonia in mice lung tissue. Methods ：48 Kunming mice were equally divided into 6 groups in random：the model, the normal group, ribavirin group, the control group, the low -moderate -high dose of Yinqiao Powder extract（20,10,5 g · kg · d^-1 ）. Except the normal group,FM1 virus was intranasally inoculated to mice. 1 h after infection, mice in control and model group were intragastrically given, mice in other group were intragastrically given the low - moderate - high and ribavirin by day 3. PR - PCR was used to measure the expressions of TLR7 - MyD88 - NF - κB mRNAin mice lung tissue. Results：Yinqiao Powder at the does of 20 and 10 g · kg · d^-1 could inhibit the mRNA expressions of TLR7 - MyD88 - NF - κB P65 （ P 〈 0.05 ）. Conclusion ： Yinqiao Powder has a very significant effect on FM1 pneumonia and the mechanism may be associate with inhibition of production of inflammatory cytokine and the expression of TLR7 - MyD88 - NF - κB signal transduction pathway.