慢性鼻-鼻窦炎（CRS)发生机制不明，涉及复杂的炎症微环境。IL-6是慢性炎症的重要调控因子，参与并放大中性粒细胞（NEU)的炎症反应，PI3K/Akt是其主要信号通路之一。GSK3β是PI3K/Akt的下游蛋白，其活化可反馈性增加IL-6的产生。本课题发现，CRS粘膜上皮中NEU的活化产物人中性粒细胞弹力蛋白酶（HNE)、IL-6、PI3K/Akt以及GSK3β的表达均较正常组织表达增高。故提出假设， IL-6- - PI3K/Akt- - GSK3β- - HNE该通路在CRS的炎症微环境中发挥重要作用，影响鼻-鼻窦粘膜细胞的凋亡、增殖,导致CRS的长期慢性炎症。本课题拟通过体内外实验，观察CRS中IL-6激活PI3K/Akt，影响GSK3β和HNE的表达，分析IL-6与GSK3β的关系，以及与HNE的关系，旨在证实课题假设，揭示CRS的可能机制。

The mechanism of chronic rhinosinusitis(CRS) is still unknown clearly,it involves complex inflammatory microenvironment.IL-6 is one of most important cytokines which participates the chronic inflammation, it Participates in and magnifies the inflammation of the neutrophils (NEU), PI3K/Akt is one of the main signaling pathways of IL-6. GSK3β is one of the downstream protein of PI3K/Akt, its activation can feedback to increase IL - 6. Our preliminary research found that the expression of human neutrophil elastic protease (HNE,the activation products of NEU), IL - 6, PI3K/Akt, as well as GSK3βin CRS mucosal epithelium, are higher than those in normal epithelium. Therefore we hypothesize that the pathway of IL - 6 - - PI3K/Akt - - GSK3β- - HNE plays a significant role in the inflammatory microenvironment of CRS, it influences the apoptosis, proliferation of rhinosinus epithelium cells and leads to a long-term inflammation of CRS.In this research, we will observe how IL - 6 activates PI3K/Akt, influences the expression of GSK3βand HNE in vivo and in vitro, and analysze the relationship between IL - 6 and GSK3β, as well as HNE.We want to reveal the possible mechanism of CRS, provides some therapeutic clues for CRS.