TLR4介导高糖调节OLP上皮细胞炎症状态的作用及机制研究

TLR4/NF-κB信号通路在多种疾病中介导炎症反应。糖尿病（DM）及口腔扁平苔藓（OLP）患者异常升高的TLR4能引起炎症相关因子TNF-α、IL-1β、IL-6合成增多，从而加重炎症反应。研究表明DM患者中OLP的发病率高于正常人，二者在病变过程中可能相互影响。而目前关于高糖环境与OLP病变的相关研究尚属空白。由此我们提出：机体高糖环境可能与OLP病损区TLR4/NF-κB介导的炎症和免疫反应存在相关性。因此，申请人拟在前期TLR4介导LPS诱导OLP上皮细胞CCL2升高的基础上，进一步明确高糖对OLP上皮细胞炎症微环境的作用，及高糖环境如何通过TLR4介导调控OLP上皮细胞炎症相关因子改变，以阐明高糖对OLP上皮细胞炎症反应的影响。预期可初步明确高糖与OLP病损炎症的关联，为今后临床上对OLP合并DM患者的治疗提供新思路。

TLR4/NF-κB pathway could induce inflammation in many diseases. Overexpression of TLR4 in Diabetes Mellitus (DM) and Oral Lichen Planus (OLP) could upregulate TNF-α, IL-1β and IL-6, and then aggravate inflammatory response. Studies revealed that the incidence of OLP in DM patients was higher than healthy group, and there may be correlation between the two diseases. But the research field of high glucose and OLP is blank till now. Therefore, we propose a hypothesis that high glucose may relate to the inflammation and immune response induced by TLR4/NF-κB in OLP. Therefore, basing on the preliminary result of TLR4 mediated LPS induced OLP epithelial cells CCL2 overexpression, the applicant plan to elucidate the effect of high glucose on the inflammatory environment in OLP epithelial cells. And explore the mechanism of high glucose on the inflammatory cytokines in OLP through TLR4 to explicate the effect of high glucose on OLP. We expected to reveal the relationship between the high glucose and inflammation in OLP lesion, and provide new viewpoint to the treatment of OLP patients combined with DM.