方法：以小鼠视网膜神经节细胞株RGC-5为研究对象，按照不同处理因素将细胞随机分为4组：正常对照组(G1)、缺氧组(G2)、缺氧+激动剂(BzATP)组(G3)、缺氧+拮抗剂(BBG)组(G4)； 采用四甲基偶氮唑蓝(MTT)法检测细胞的存活率； 用Annxin V/PI染色流式细胞术检测细胞凋亡率； Western Blot检测细胞内cleave-caspase-3和cleave-PARP蛋白的表达。

结果：与正常对照组相比，RGC-5细胞经缺氧处理后，细胞存活率明显降低； 凋亡率显著升高； 细胞内cleave-caspase-3和cleave-PARP蛋白表达增加； P2X₇受体激动剂BzATP能明显加重缺氧诱发的细胞凋亡，而BBG预处理可以显著拮抗缺氧所致的细胞凋亡。

结论：缺氧能激活视网膜神经节细胞嘌呤受体P2X₇，并参与视网膜神经节细胞的凋亡。

METHODS: According to the different factors, retinal ganglion cells of the mouse were randomly divided into four groups: control group(G1), hypoxia group(G2), hypoxia + agonist(BzATP)group(G3), hypoxia + antagonistic agent(BBG)group(G4). Methyl thiazolyl tetrazolium(MTT)method was used to detect the survival rate of cells; the rate of cell apoptosis was determined by Annxin V/PI staining flow cytometry; Western Blot analysis was employed to detect the protein expressrion levels of cleave-caspase-3 and cleave-PARP.

RESULTS: Compared with control group, the results significantly indicated the survival rate of cells decreased and the rate of apoptosis increased treated with hypoxia. In addition, the protein levels of cleave-caspase-3 and cleave-PARP were remarkably higher than the control group. BzATP markedly augmented the apoptosis induced by hypoxia, and BBG pretreatment observably decreased the hypoxia-induced apoptosis.

CONCLUSION: P2X₇ purinoceptor could be activated by hypoxia, and participate in the apoptosis of retinal ganglion cells.