亚炎症是机体对于应激及功能失衡的一种适应性反应，小胶质细胞激活是其特点之一，然而持续存在或者过度反应的亚炎症是促使慢性退行性疾病发生发展的一个重要机制。我们的前期工作表明，小胶质细胞在视网膜内层有分布，且缺血再灌注能够诱导小胶质细胞的激活。本课题提出科学假说：1）亚炎症及小胶质细胞的激活存在于青光眼的发生发展中；2）调控TLR2/4通路及小胶质细胞的激活，进而控制亚炎症，可能成为青光眼干预的有效靶点。本课题主要通过体内动物实验并结合临床标本，探讨TLR2/4通路介导的小胶质细胞激活及亚炎症在青光眼性视神经病变中的作用。藉此研究，有望调控亚炎症能作为青光眼早期干预的有效靶点。本课题首次将亚炎症概念引入青光眼研究领域，将从全新的角度探索青光眼的发病机制，并为早期干预提供新的途径，是十分值得探索的课题。

Para-inflammation is an adaptive response when tissues subjecting to malfunction, which is also the intermediate between basal and inflammatory states. The major characteristic of para-inflammation is microglia cell activation, and sustained para-inflammation is associated with many chronic degenerative diseases. Our previous work found that microglia cell located at the inner layer of retina, and retina ischemia-reperfusion induced microglia cell activation. Based on above, we put forward our hypothesis: 1)para-inflammation and microglia cell activation play a key role in the pathogenesis and development of glaucoma;2)regulating the TLR2 or TLR4 pathway and alleviating microglia cell activation in order to mitigate the para-inflammation may be an effective way to treat glaucoma. In this study, we planned to use animal models and clinical samples to verify our hypothesis. The purpose of this study is to provide a brand new view to the pathogenesis of glaucoma. We also hope to find a new way to the early prevention of the glaucoma.