CircBPTF knockdown ameliorates high glucose-induced inflammatory injuries and oxidative stress by targeting the miR-384/LIN28B axis in human umbilical vein endothelial cells.

Endothelial dysfunction is a primary cause of diabetes-related vascular complications, such as atherosclerosis. Accumulated research indicates that circular RNAs (circRNAs) are involved in the pathogenesis of cardiovascular disease. This study intended to explore the function and mechanism of circBPTF in high glucose (HG)-induced vascular inflammatory models. Cell model of inflammatory injury was established in human umbilical vein endothelial cells (HUVECs) with HG treatment. The expression of circBPTF, miR-384 and lin-28 homolog B (LIN28B) was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability and apoptosis were assessed by cell counting kit-8 (CCK-8) and flow cytometry assay, respectively. The expression of LIN28B was also examined using western blot. The release of proinflammatory cytokines was detected by enzyme-linked immunosorbent assay (ELISA). The production of ROS, SOD and MDA was detected to assess oxidative stress. The target relationship was predicted by bioinformatics analysis and verified using dual-luciferase reporter assay and RIP assay. CircBPTF was highly regulated in HG-induced HUVECs. CircBPTF knockdown increased cell viability and suppressed cell apoptosis, the release of proinflammatory cytokines and oxidative stress in HG-induced HUVECs. MiR-384 was targeted by circBPTF, and its downregulation abolished the effects of circBPTF knockdown. Moreover, circBPTF positively regulated LIN28B expression via targeting miR-384. Overall, CircBPTF knockdown protected against HG-induced inflammatory injuries and oxidative stress by mediating the miR-384/LIN28B axis in HUVECs. Our study provides a feasible theoretical strategy for preventing vascular cell dysfunction.