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目的:评价n hsa_circ_0081596在人神经细胞氧糖剥夺/复糖复氧(OGD/R)损伤中的作用。n 方法:培养人神经母细胞瘤细胞，采用随机数字表法将细胞(5代以内)分为4组(n n＝20)：对照组(C组)、OGD/R组(O组)、OGD/R+小干扰RNA(siRNA)组(S组)、OGD/R+siRNA阴性对照组(I组)。C组细胞在37 ℃、5%COn 2正常条件下培养，O组细胞铺于6孔板或96孔板待完全贴壁，氧糖剥夺4 h后复糖复氧24 h制备OGD/R损伤模型。S组和I组分别转染n hsa_circ_0081596 siRNA及其阴性对照，72 h后建立OGD/R模型。采用qRT-PCR法测定n hsa_circ_0081596和线粒体分裂蛋白1(Fis1)mRNA的表达水平，采用Western blot发测定Fis1的表达水平，采用CCK-8法确定细胞存活率，采用流式细胞仪检测细胞凋亡率。n 结果:与C组比较，O组n hsa_circ_0081596、Fis1及其mRNA表达上调，细胞存活率降低，凋亡率升高(n P0.05)。n 结论:hsa_circ_0081596可通过上调Fis1表达参与人神经细胞OGD/R损伤的病理生理机制。n “,”Objective:To evaluate the role of n hsa_circ_0081596 in oxygen-glucose deprivation and restoration (OGD/R) injury to human neurons.n Methods:SK-N-SH cells were cultured and the cells within 5 generations were divided into 4 groups (n n=20 each) using a random number table method: control group (group C), OGD/R group (group O), OGD/R+ siRNA group (group S) and OGD/R+ siRNA negative control group (group I). The cells in C group were cultured under normal conditions of 37 ℃ and 5% COn 2.The cells in group O were placed in 6- or 96-well plates until they were completely attached to the wall, and then subjected to oxygen-glucose deprivation for 4 h, followed by restoration of oxygen-glucose for 24 h. In group S and group I, the cells were transfected with n hsa_circ_0081596 siRNA and its negative control, respectively, and 72 h later OGD/R model was established.The expression of n hsa_circ_0081596 and mitochondrial fission protein 1 (Fis1) mRNA was detected using quantitative real-time polymerase chain reaction.The expression of Fis1 was determined by Western blot, the cell survival rate was determined by CCK-8 assay and the apoptosis rate was determined by flow cytometry.n Results:Compared with group C, the expression of n hsa_circ_0081596, Fis1 and its mRNA was significantly up-regulated, the cell survival rate was decreased, and the apoptosis rate was increased in group O (n P0.05).n Conclusion:hsa_circ_0081596 is involved in the pathophysiological mechanism of OGD/R through up-regulating the expression of Fis1 in human neurons.n