腺苷作为一种生物活性物质，其对青光眼视网膜神经节细胞（RGCs）的损伤是否具有保护作用，及其对青光眼视网膜Müller细胞的钾离子通道和谷氨酸转运功能的影响目前尚未完全阐明。我们前期的初步研究发现腺苷具有调控加压培养视网膜Müller细胞的钾离子通道的作用，由此本项目将采用在体大鼠慢性高眼压模型和Müller细胞加压培养及谷氨酸毒性作用培养的体外实验，进一步探讨青光眼状态下视网膜Müller细胞的钾离子通道的改变及其与RGCs损伤的关系，研究腺苷对青光眼状态下视网膜Müller细胞的钾离子通道、谷氨酸转运功能和RGCs存活的影响，同时进一步探讨腺苷对实验性青光眼状态下视网膜Müller细胞的钾离子通道影响的可能作用途径，以初步明确腺苷对青光眼RGCs的保护作用及其机制，为发掘青光眼的视神经保护方法和治疗靶点提供实验依据，丰富青光眼视神经损害的作用机制，对提高学科水平和社会效益均有重要意义。

Adenosine is a biological active substance. It has not yet been fully elucidated whether adenosine has a protective effect for retinal ganglion cells (RGCs) damage of glaucoma. The effects of adenosine on potassium ion channels and glutamate transport function of retinal Müller cells in glaucoma have also not yet been fully understood. In the preliminary study, we found that adenosine has the effect of potassium ion channels regulation on retinal Müller cells culture in vitro under the pressure condition. Thus, we will use rat model in vivo with chronic high intraocular pressure and retinal Müller cells culture in vitro under the pressure condition or glutamate toxicity stimulation to study the changes of potassium ion channels of retinal Müller cells in glaucoma condition, and explore the relationship between the changes of potassium ion channels and RGCs damage. On the other hand, the effects of adenosine on potassium ion channels and glutamate transport function of retinal Müller cells, and RGCs survival in glaucoma condition will be investigated. Furthermore, the possible effect pathway of adenosine on potassium ion channels of retinal Müller cells in glaucoma condition will also be explored. This project will preliminary clarify the RGCs protective effect of adenosine and its mechanism. The expected results of this project will provide the experimental evidences for excavating the treatment method and target of neuroprotection, and enrich the glaucomatous optic nerve damage mechanisms, which has the important significance for improving the academic levels and social benefits.