摘要
目的:探讨嘌呤受体P2X_7对缺氧诱发小鼠视网膜神经节细胞凋亡的影响。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cleavecaspase-3和cleave-PARP蛋白表达增加;P2X_7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P2X_7,并参与视网膜神经节细胞的凋亡。
AIM：To investigate the effect of P2X7 on hypoxiainduced apoptosis of retinal ganglion cells in mice.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 cleavePARP.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.
出处
《国际眼科杂志》
CAS
2016年第4期622-624,共3页
International Eye Science
基金
辽宁省自然科学基金(No.2014020184)~~
