| Popis: |
To explore the influence and mechanism of lncRNA SNHG14 on oxidized low-density lipoprotein (oxLDL)-induced vascular endothelial cell injury, cellular levels of SNHG14 and miRNA-93-5p were detected in oxLDL-induced vascular endothelial cells by RT-qPCR, and the levels of MDA, SOD and GSH-Px were detected by ELISA. Flow cytometry was used to detect cellular apoptosis, and western blot analysis was used to determine the abundance of Bcl-2 and Bax proteins. SNHG14 small interfering RNA or miRNA-93-5p mimics were transfected into vascular endothelial cells to interfere with SNHG14 expression or overexpress miRNA-93-5p. To study the effects of interfering with SNHG14 expression or overexpression of miRNA-93-5p, the levels of MDA, SOD and GSH-Px, apoptosis and the levels of Bcl-2 and Bax protein were studied in oxLDL-induced endothelial cells with either altered SNHG14 expression or overexpressed miRNA-93-5p. A dual-luciferase reporter gene experiment verified the regulatory connection between SNHG14 and miRNA-93-5p. After oxLDL acted on vascular endothelial cells, the expression levels of SNHG14 were significantly increased, while the expression levels of miRNA-93-5p were significantly reduced, MDA levels were increased, and SOD and GSH-Px activities were reduced. Both the apoptosis rate and Bax protein levels were significantly increased, and Bcl-2 expression was reduced. Interference with SNHG14 expression or overexpression of miRNA-93-5p can reduce the MDA content in oxLDL-induced vascular endothelial cells, increase the activity of SOD and GSH-Px, and reduce the apoptosis rate and Bax protein levels, and promote Bcl-2 expression. SNHG14 targeted to negatively regulate miRNA-93-5p expression, inhibited miRNA-93-5p expression and reversed the interference of SNHG14 expression with oxLDL-induced variation in MDA, SOD and GSH-Px levels, apoptosis rate, and Bax and Bcl-2 protein levels. Interference of SNHG14 expression may reduce oxidative stress and apoptosis of vascular endothelial cells induced by oxLDL by negatively regulating the expression of miRNA-93-5p. |
