The effect of miR-532-5p on human brain microvascular endothelial cells damage induced by ox-LDL is studied. HBMEC-3 were cultured and treated with ox-LDL for 24 h to establish a model of cell oxidative damage. The expression of miR-532-5p was detected by qRT-PCR and that of CLIC4 was detected by Western blot. miR-NC, miR-532-5p mimics, si-NC, si-CLIC4, miR-532-5p mimics and pcDNA, miR-532-5p mimics and pcDNA-CLIC4 were transfected into HBMEC-3 cells, respectively, using ox -LDL processing for 24 h. Flow cytometry was used to detect the apoptotic rate. The dual luciferase reporting experiment verified the relationship between miR-532-5p and CLIC4. The ox-LDL treatment led to lower expression of miR-532-5p (p<0.05), higher expression of CLIC4 (P <0.05), enhanced content of MDA (p<0.05), decreased activities of SOD and CAT (p<0.05), increased apoptosis rate (p<0.05), higher protein level of Bax (p<0.05), and lower protein level of Bcl-2 (p<0.05). Compared with ox-LDL + miR-NC group and ox-LDL + si-NC group, ox-LDL + miR-532-5p group and ox-LDL + si-CLIC4 group had decreased content of MDA (P<0.05), increased activities of SOD and CAT (p<0.05), decreased apoptosis rate (p<0.05), lower level of Bax (p<0.05), and higher level of Bcl-2 (p<0.05). The miR-532-5p mitigates human brain microvascular endothelial cells damage induced by ox-LDL via down-regulating CLIC4 expression.