Toll样受体4信号途径在大鼠中耳积液中的表达

目的探讨Toll样受体4（Toll like receptor 4,TLR4）信号途径在中耳积液大鼠的作用机制。方法采用听泡内注入纤维蛋白封闭剂和脂多糖制作大鼠中耳积液模型。分别于3、5、7、9、11、13天处死大鼠,每次5只。取中耳黏膜检测TLR4、诱生型一氧化氮合酶（inducible nitric oxide synthase,iNOS）、白细胞介素8（interleukin-8,IL-8）mRNA的表达;免疫组化检测核因子κB（nuclear factor kappa B,NF-κB）表达情况。结果对照组中耳黏膜内有少量的TLR4、iNOS和IL-8mRNA的表达,中耳积液时表达量明显增高（P〈0.05）。免疫组化检测显示大鼠中耳黏膜内NF-κBp65的表达在中耳积液时明显提高。结论中耳积液时TLR4表达明显升高,并伴有NF-κB活化,促进下游IL-8等的表达,可能是引发大鼠分泌性中耳炎的机制之一。

The expression of TLR4 signaling pathway in rat with secretory otitis media

OBJECTIVE To investigate the role of TLR4 signaling pathway in secretory otitis media of rats.METHODS Rats SOM models were made by infusing FS and LPS to the middle otocysts. The rats were killed separately at the 3rd, 5th, 7th, 9th,11th and13th day（5 rats each time）. And then the expressions of TLR4, iNOS, IL-8mRNA of middle ear mucosae were detected. NF-κB was also detected through the method of immunohistochemistry. RESULTS The expressions of TLR4mRNA, iNOS and IL-8mRNA in middle ear mucosae of SOM group were significantly higher than that of control group. Immunohistochemistry method showed that the activation of NF-κB in middle ear mucosae was obviously increased in SOM. CONCLUSION The expression of TLR4 was obviously increased in SOM and it activates the NF-κB, promotes the expression of downstream IL-8. That maybe the mechanism which cause SOM.