Objective　To investigate the mechanism of CirCDC14A silencing to protect astrocytes from oxygen-glucose deprivation/glyco-reoxygenation (OGD/R)-induced injury by regulating the miR-153-3p/JAK1 axis.Methods　Cerebral cortical astrocytes of neonatal rats were cultured in vitro,and the cell viability was detected by CCK-8 method;annexin V-FITC/PI staining was used to detect cell apoptosis.Western blot method was used to detect the protein expression levels of p53,Bax and Bcl-2 in each group,and the relationship between CirCDC14A and miR-153- 3p,miR-153-3p and JAK1 was analyzed by dual-luciferase reporter gene assay.Results　The cell viability increased with time; the cell viability of pcDNA3.0 CirCDC14A+si JAK1 group at 48 h and 72 h was lower than that of si-NC group,OGD/R group and OGD/R+Si+Con mimcs group (P<0.05);compared with si-NC group,the apoptosis of OGD/R group,OGD/R+Si+Con mimcs group,pcDNA3.0-CirCDC14A+si JAK1+miR-153-3p mimcs group increased significantly,and pcDNA3.0-CirCDC14A+si JAK1+miR-153-3p mimcs group had higher apoptosis than OGD/R+Si+Con mimcs group (P<0.05);Western blot results showed that:pcDNA3.0-CirCDC14A+si JAK1+miR,the protein expression levels of p53,Bax and Bcl-2 in the miR-153-3p mimcs group were lower than those in the OGD/R group,OGD/R+Si+Con mimcs group and si-NC group (P<0.05).Reduced the luciferase activity of CirCDC14A WT and JAK1-WT (P<0.05); the level of miR-153-3p in the pcDNA3.0-CirCDC14A+si JAK1+miR-153-3p mimcs group was lower than that in the other three groups (P<0.05). The JAK1 protein level was higher than the other three groups (P<0.05).Conclusion　CirCDC14A gene silencing may inhibit OGD/R-induced apoptosis of rat astrocytes by regulating the miR-153-3p/JAK1 axis,resulting in decreased cell viability and protein expression levels of p53,Bax and Bcl-2.