大气污染中的颗粒物（PM）对眼表有明显的损害作用，但其分子机制尚不完全清楚。我们前期研究表明，PM可通过调控炎症、氧化、凋亡等过程诱发小鼠类似干眼的眼表损伤；而维生素D(VD)可以促进人角膜上皮（HCE）细胞的增殖,抑制PM损伤的HCE细胞中caspase-1的表达。据此我们提出假设：NOX4/ROS/NLRP3信号通路可能参与PM对眼表的损伤作用,而这种损伤作用可能会被VD抑制。本项目拟在PM损伤的细胞及小鼠动物模型，利用形态学、生物分子学及体内检测等手段，研究NOX4/ROS/NLRP3信号通路在PM损伤眼表过程中的作用及相关分子机制；同时探讨VD对PM眼表损伤的抑制效应及对相关信号通路的调控作用，以期阐明VD通过NOX4/ROS/NLRP3信号通路抑制PM对眼表的损伤作用。本项目的研究结果将为大气污染所致的眼表损伤的治疗和预防提供新的思路和靶点。

Particulate matter (PM) of air pollution can damage ocular surface, but the exact mechanism of ocular damage induced by PM is unknown. Our previous studies found that PM induced the ocular damage resembling dry eye by regulating processes including inflammation, oxidation, and apoptosis, and VD stimulated proliferation of corneal epithelial (HCE) cells and down-regulated the caspase-1 expression of HCE cells intervented by PM increased significantly. Thus, we propose the hypothesis that NOX4/ROS/NLRP3 signaling pathway play the key role in ocular damage induced by PM and VD attenuates PM-ocular damage. In this study, we will take advantage of the morphology, molecular biology and vivo detection technologies to study the key role of NOX4/ROS/NLRP3 signaling pathway playing in ocular damage induced by PM. And the effect of VD on the ocular damage induced by PM and the expression of NOX4/ROS/NLRP3 signaling pathway factors would be investigated to clarify VD attenuates PM-ocular damage via the signaling pathway described above. This project may provide a novel thought and target for clinical treatment and prevention of ocular diseases induced by air pollution.