Aim To investigate the effect of miR-152-3p targeting thioredoxin-interacting protein (TXNIP) on the apoptosis of endothelial progenitor cells (EPC) induced by hydrogen peroxide (H₂O₂). Methods Endothelial progenitor cells were isolated from the peripheral blood of healthy people and identified, a H₂O₂-induced endothelial progenitor cells damage model (500 μmol/L H₂O₂ treated for 8 h) was established and the expression of miR-152-3p in endothelial progenitor cells was detected by RT-qPCR. After overexpression of miR-152-3p or inhibition of TXNIP expression or overexpression of miR-152-3p and TXNIP simultaneously in endothelial progenitor cells, they were treated with 500 μmol/L H₂O₂ for 8 h, the expression level of miR-152-3p, cell apoptosis rate and TXNIP, Bax, Bcl-2, and Caspase-3 protein expression levels were measured; dual luciferase reporter gene experiment was performed to verify the relationship between miR-152-3p and TXNIP. Results Endothelial progenitor cells were successfully isolated from the peripheral blood of healthy people, and the expression level of miR-152-3p in H₂O₂-induced endothelial progenitor cells decreased by 65.0% (P＜0.001). Compared with the control group, the apoptosis rate, Bax and Caspase-3 protein expression levels in the model group increased by 895.1%, 352.0% and 290.3%, and the Bcl-2 expression level decreased by 79.4% (all P＜0.001). Compared with the miR-NC group, the apoptosis rate and the protein expression levels of Bax and Caspase-3 in the miR-152-3p mimic group decreased by 55.7%, 60.9% and 56.8% (P＜0.001), and the protein expression level of Bcl-2 increased by 389.5% (all P＜0.001). Compared with the si-NC group, the apoptosis rate and the protein expression levels of TXNIP, Bax and Caspase-3 in the si-TXNIP group were decreased by about 40.2%, 57.5%, 59.8% and 55.4% (all P＜0.001). Compared with miR-152-3p mimic＋pcDNA group, the apoptosis rate, TXNIP, the protein expression levels of Bax and Caspase-3 increased by 86.8%, 184.8%, 137.7% and 109.2% (P＜0.001), and the protein expression level of Bcl-2 decreased by 69.1% (P＜0.001). The results of dual luciferase reporter gene experiments showed that miR-152-3p was able to target and negatively regulate TXNIP expression. Conclusion MiR-152-3p was under-expressed in H₂O₂-induced endothelial progenitor cells. Overexpression of miR-152-3p can inhibit H₂O₂-induced endothelial progenitor cell apoptosis by targeting the expression of TXNIP.