视网膜神经节细胞（RGC）的凋亡和神经轴突的退变是诸多视神经视网膜疾病的重要病理过程。RGC凋亡涉及机制复杂，包括组织缺血缺氧、胶质细胞活化、营养因子缺乏、兴奋性毒性氨基酸释放等。我们前期研究表明，PPAR-γ配体匹格列酮能够有效保护大鼠急性缺血再灌注损伤过程中视网膜形态及功能损伤，增加RGC存活率，抑制损伤所造成的视网膜细胞凋亡，并且在该病理过程中能够显著抑制胶质细胞激活。由此我们提出假设：匹格列酮对RGC缺氧损伤具保护作用，该作用可能同时通过对RGC本身及其周围微环境两种作用途径实现。其机制可能与干预细胞凋亡、氧化应激过程中关键信号通路调控元件及对Müller细胞功能的调控有关。本研究以原代视网膜神经节细胞结合视网膜植片培养技术为研究模型进一步深入，阐明匹格列酮对低氧诱导RGC损伤保护的作用方式及其机制，为其最终能够在临床上以新的神经保护制剂应用于视神经视网膜疾病奠定实验基础。

Retinal ganglion cell (RGC) apoptosis and the degeneration of its axons are important pathological processes of many retinal and optic nerve associated diseases. The mechanism for apoptosis of RGC involves ischemia and hypoxia, glial activation, neurotrophic factors deprivation, excitotoxic damage and so on. Our preliminary research suggests that the PPAR-γ ligand pioglitazone effectively protected the retina during acute ischemia-reperfusion (I/R) injury in rat against morphological and functional damages. Including increased RGC survival, inhibition of retinal cell apoptosis caused by I/R injury, as well as the significant inhibition of glia activation during the pathological process. We put up an assumption that pioglitazone could protect RGC against hypoxic injury, by the effect that both directly towards the RGC itself and also the microenvironment surrounded. Mechanism might lies in the regulation of certain factors that involve in cell apoptosis and oxidative stress associated signaling pathways and the Müller cell function regulation. This study based on the ex-vivo model of retinal ganglion cells culture and combined with retinal implant techniques would further clarifying the way and mechanism of the protective effect of pioglitazone on hypoxia-induced RGC injury, which might serve as an experimental basis for clinical use of pioglitazone as a new neuroprotective agents applied to the retinal and optic nerve associated diseases.