Abstract: Objective To investigate the effect of long non-coding RNA ( lncRNA) homologous anomalous box gene A11 antisense RNA (HOXA11-AS) on oxidative low density lipoprotein (ox-LDL) induced vascular endothelial cells injury by targeting micrornA-766-3p (miR-766-3p). Methods Human umbilical vein endothelial cells (HUVEC) were treated with 100 μg / mL ox-LDL for 24 hours to establish a cell injury model. HUVEC were divided into the control ( con) group, ox-LDL group, ox-LDL + si-NC group, ox-LDL + si-HOXA11-AS group, ox-LDL + miR-NC group, ox-LDL + miR-766-3p group, ox-LDL + si-HOXA11-AS + anti-miR-NC group, and the ox-LDL + si-HOXA11-AS + anti-miR-766-3p group. Expression of HOXA11-AS and miR-7666-3p was assessed by RT-qPCR. Cell apoptosis was detected using flow cytometry. The kits detected LDH release and intracellular SOD activity. ELISA method was used to calculate the levels of TNF-α and IL-1β in the culture medium. Dual luciferase reporter assay was used to confirm the targeting relationship between HOXA11-AS and miR-766-3p. Results Compared with the control group, the HUVEC cell apoptosis rate, LDH release, HOXA11-AS expression, and the levels of TNF-α and IL-1β in the culture medium of the ox-LDL group were significantly increased (P< 0. 05), the SOD activity and the miR-766-3p expression level were significantly reduced (P< 0. 05). Compared with the ox-LDL + si-NC group, the HUVEC cell apoptosis rate, LDH release, and the levels of TNF-α and IL-1β in the culture medium of the ox-LDL + si-HOXA11-AS group were significantly reduced (P< 0. 05), the SOD activity was significantly increased ( P < 0. 05). Compared with the ox-LDL + miR-NC group, the HUVEC cell apoptosis rate, LDH release, and the levels of TNF-α and IL-1β in the culture medium of the ox-LDL + miR-766-3p group were significantly reduced ( P < 0. 05), the SOD activity was significantly increased ( P < 0. 05 ). miR-766-3p is the a target of HOXA11- AS. Compared with the ox-LDL + si-HOXA11-AS + anti-miR-NC group, the HUVEC cell apoptosis rate, LDH release, and levels of TNF-α and IL-1β in the culture medium of the ox-LDL + si-HOXA11-AS + anti-miR-766-3p group were significantly increased (P< 0. 05), and the SOD activity was significantly decreased (P< 0. 05). Conclusion Silencing HOXA11-AS inhibits ox-LDL-induced vascular endothelial cell apoptosis, oxidative stress and inflammation by up-regulating the expression ofmiR-766-3p. 

Key words: vascular endothelial cells, oxidized low-density lipoprotein, HOXA11-AS, miR-766-3p, apoptosis, oxidative stress, inflammation