Abstract

This study aimed to investigate the effect of lncRNA SNHG15 targeting miR-362-3p on LPS-induced vascular endothelial cell apoptosis, inflammatory factor expression and oxidative stress. For this purpose, human umbilical vein endothelial cells (HUVECs) were treated with 100 ng/mL LPS for 24 hours to establish a cell injury model. HUVECs were divided into control, LPS, LPS+si-NC, LPS+si-SNHG15, LPS+miR-NC, LPS+miR-362-3p, LPS+si-SNHG15+anti-miR-NC and LPS+si-SNHG15+anti-miR-362-3p groups. RT-qPCR was used to determine SNHG15 and miR-362-3pexpression. The cell inhibition rate was measured by the CCK-8 method; Cell apoptosis rate was detected by flow cytometry; the kits were employed to detect the intracellular SOD activity and the release of LDH; the ELISA method was applied to detcet the levels of TNF-α, IL-6 and IL-10 in the culture medium. Results showed that compared with the control group, the inhibition rate, apoptosis rate and SNHG15 expression level of HUVECs in the LPS group were increased (P<0.05), and the levels of TNF-α, IL-6 and LDH in the culture medium were increased (P<0.05), SOD activity, miR-362-3p expression level, and IL-10 level in the culture medium were reduced (P<0.05). The inhibition rate and apoptosis rate of HUVECs in the LPS+si-SNHG15 group were reduced (P<0.05), and the levels of TNF-α, IL-6 and LDH in the culture medium were reduced (P<0.05), SOD activity and IL-10 levels in the culture medium increased (P<0.05). The inhibition rate and apoptosis rate of HUVECs in the LPS+miR-362-3p group were reduced (P<0.05), and the levels of TNF-α, IL-6 and LDH in the culture medium were reduced (P<0.05), SOD activity and IL-10 level in the culture medium increased (P<0.05). miR-362-3p directly and bound to SNHG15. Compared with the LPS+si-SNHG15+anti-miR-NC group, the inhibition rate and apoptosis rate of HUVECs in the LPS+si-SNHG15+anti-miR-362-3p group were increased (P<0.05), and the levels of TNF-α, IL-6 and LDH in the culture medium were increased (P<0.05), and SOD activity and IL-10 levels in the culture medium were reduced (P<0.05). In general, silencing lncRNA SNHG15 inhibited LPS-induced vascular endothelial cell apoptosis, inflammatory factor expression and oxidative stress response by up-regulating miR-362-3p expression.

Highlights

  • This study aimed to investigate the effect of lncRNA SNHG15 targeting miR-362-3p on LPS-induced vascular endothelial cell apoptosis, inflammatory factor expression and oxidative stress

  • The cell inhibition rate was measured by the CCK-8 method; Cell apoptosis rate was detected by flow cytometry; the kits were employed to detect the intracellular Superoxide dismutase (SOD) activity and the release of Lactate dehydrogenase (LDH); the ELISA method was applied to detcet the levels of tumor necrosis factor (TNF)-α, IL-6 and IL-10 in the culture medium

  • Results showed that compared with the control group, the inhibition rate, apoptosis rate and SNHG15 expression level of human umbilical vein endothelial cells (HUVECs) in the LPS group were increased (P

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Summary

Introduction

This study aimed to investigate the effect of lncRNA SNHG15 targeting miR-362-3p on LPS-induced vascular endothelial cell apoptosis, inflammatory factor expression and oxidative stress. For this purpose, human umbilical vein endothelial cells (HUVECs) were treated with 100 ng/mL LPS for 24 hours to establish a cell injury model. The inhibition rate and apoptosis rate of HUVECs in the LPS+si-SNHG15 group were reduced (P

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