视网膜缺血/再灌注损伤后干预措施仅仅针对视网膜神经元损伤机制不足以恢复受损的视功能。我们的前期研究发现:在缺血/在灌注损伤后早期，视网膜神经元之间突触结构、功能蛋白表达异常，并伴随着视功能的退化。活化的星形胶质细胞参与调控了这一过程。以往的研究表明:星形胶质细胞活化可呈现出不同的功能极化表型，主要为神经毒性型(M1型)和神经保护型(M2型)。进一步发现视网膜缺血/再灌注损伤后早期星形胶质细胞以M1型为主，且伴随着介导其M1型功能表型极化的关键分子lipocalin-2(LCN2)的表达上调。我们推测:LCN2介导的M1型星形胶质细胞调控了视网膜缺血/再灌注损伤后早期视网膜神经元之间突触的重塑，这可能 是造成视功能障碍的重要原因之一。本项目将探索LCN2介导的星形胶质细胞功能表型极化在视网膜缺血/再灌注损伤后突触重塑和视功能障碍中的作用及机制，为相关疾病视功能恢复提供新的干预时间和靶点。

Intervention measures which only compete against the mechanisms of neuronal injury in retinae can not recover the degenerated visual function following retinal ischemia/reperfusion (I/R) injury. We previously found that the degenerated visual function preceded the I/R induced neuronal death in retinae, which accompanied the synaptic remodeling on the visual signal pathway. And the activated astrocytes mediated these events. Previous studies from other groups indicated that the activated astrocytes can present dual function—neurotoxic effect (M1) and neuroprotective effect (M2). Further explorations showed that the activated astrocytes presented the neurotoxic effect(M1) following retinal I/R injury. Meanwhile, the key molecule for phenotypic polarization of M1 astrocytes，lipocalin-2 (LCN2), up-regulated. We speculate that LCN 2 induced phenotypic polarization of M1 astrocytes mediates the synaptic remodeling and visual dysfunction following retinal I/R injury, which may be one of the key reasons for the visual dysfunction following retinal I/R injury. The present study will investigate the roles and the potential molecular mechanisms of LCN2 induced phenotypic polarization of M1 astrocytes in the synaptic remodeling and visual dysfunction following retinal I/R injury. We try to provide new evidences to retinal repair strategies for better visual function recovery on intervention time points and new targets.