Expression of LncRNA DLGAP1-AS1 in a Mouse Model of Atherosclerosis and Its Effect on Oxidized Low-Density Lipoprotein-Induced Vascular Endothelial Cell Injury

Abstract

The occurrence of vascular endothelial injury is key to the progression of atherosclerosis (AS). This research explores the expression of lncRNA DLGAP1-AS1 in a mouse model of atherosclerosis and its effect on ox-LDL-induced vascular endothelial cell injury. A mouse model of AS was constructed, and DLGAP1-AS1 expression was detected using the nano real-time PCR method. Vascular endothelial cells (VEC) are categorized into four groups. Flow cytometry detects cell apoptosis, and Western blot detects Bax and Bcl-2 expressions; WST-8 method detects level of SOD. Thiobarbituric acid method, Ammonium molybdate colorimetric method, DCFH-DA method were used to detect MDA, CAT, and reactive oxygen species (ROS) levels, respectively. Bioinformatics software predicted the target genes of DLGAP1-AS1. DLGAP1-AS1 expression was raised in AS mice, apoptotic rate and Bax expression in the ox-LDL group were raised, Bcl-2 expression was abated, MDA and ROS levels were raised, SOD and CAT levels were abated than in control. The si-DLGAP1-AS1+ox-LDL group decreased cell death and Bax expression, increased Bcl-2 expression, decreased MDA and ROS levels, and increased SOD and CAT levels than in the si-NC+ox-LDL group. Down-regulation of DLGAP1-AS1 was targeted in order to promote miR-26a-5p expression. Compared with co-transfection with DLGAP1-AS1 siRNA and inhibitor control, the apoptosis rate and Bax expression were increased after co-transfection with DLGAP1-AS1 siRNA and miR-26a-5p inhibitor, Bcl-2 expression was decreased, and MDA and ROS levels were increased, the level of SOD and CAT were decreased. DLGAP1-AS1 was up-regulated in AS mice and downregulated to promote miR-26a-5p to inhibit ox-LDL-induced vascular endothelial cell death and oxidative damage.