流感病毒性肺炎湿热证小鼠TLR-7介导信号通路的变化

Changes of TLR-7 Signal Pathway of Influenza Viral Pneumonia Mice with Damp-he at Syndrome

目的通过人工气候模拟,观察流感病毒性肺炎湿热证小鼠Toll样受体7(TLR-7)介导信号通路的变化,探讨病毒性疾病湿热证的物质基础。方法将50只BALB/c小鼠随机分为正常对照组10只、单纯湿热组10只、湿热模型组15只、单纯病毒组15只。单纯湿热组:全程高脂饲料喂养,连续10天置于气候箱;湿热模型组:全程高脂饲料喂养,连续10天置于气候箱,第11天接种病毒,接种病毒后不再置入气候箱;单纯病毒组:全程普通饲料喂养14天,不置入气候箱,第11天接种病毒1次,继续喂养3天,第15天处死采集标本,每组随机选取8个样本检测,比较各组TLR-7、核因子-κB(NF-κB)、髓样分化因子88(MyD88)mRNA表达水平。结果湿热模型组TLR-7、MyD88、NF-κB三者mRNA表达水平较其他3组增高,但TLR-7、MyD884组间差异无统计学意义(P>0.05),NF-κB水平湿热模型组高于其他3组(P<0.05或P<0.01)。结论湿热因素干预能上调TLR-7介导信号因子,尤其是下游信号因子NF-κB,从而激发Tol1-NF-κB信号通路,导致湿热模型组小鼠肺脏病变程度较单纯病毒组重。

Objective To explore the characteristic of damp-heat syndrome of viral diseases through observing the changes of signal pathway induced bY TLR-7 transduction in mice with damp-heat syndrome of influenza viral pneumonia. Methods Fifty BALB/c mice were randomized into control group （10 mice）, damp-heat group （10 mice）, model group （15 mice）, and viral group （15 mice）. The damp-heat group was fed with high-fat feed for the whole experimental process and put into the climate box for 10 days in succession. The model group was fed with high-fat feed for the whole experimental process, put into the cli- mate box for 10 days in succession, and vaccinated with virus on the 11th day, then not back to the climate box again. The viral group was fed with normal feed for 14 days, not put into the climate box, and vaccinated with virus on the 11th day once, then fed for 3 days again. The animals were sacrified on the 15th day, 8 samples were randomly selected from each group to detect the expression of TLR-7, NF-xB, and MyD88 mRNA. Results The expressions of TLR-7, MyD88, and NF-xB in the model group were higher than those in the viral group, but the difference of TLR-7 and MyD88 expressions in these two groups was not statistically significant, however the difference NF-xB expression was statistically significant. The up-regulated amplitude of the three wasn＇t parallel. Conclusion Intervention with damp-heat may increase the TLR-7 signal factors, especially NF- tcB, which is the lower reach of pathway, thus aroused the Toll-NF-xB signal pathway, leading to a more severe pathological condition and the higher mortality of mice with damp-heat syndrome.