Effect of lncRNA SNHG15 on LPS-induced vascular endothelial cell apoptosis, inflammatory factor expression and oxidative stress by targeting miR-362-3p

被引:8
|
作者
Liu, Guanghai [1 ]
Tian, Rong [1 ]
Mao, Hengchao [1 ]
Ren, Yanping [2 ]
机构
[1] Zunyi Med Univ, Morphol Lab, Zunyi 563000, Guizhou, Peoples R China
[2] Zunyi Med Univ, Dept Histol & Embryol, Zunyi 563000, Guizhou, Peoples R China
关键词
Human umbilical vein endothelial cells; Lipopolysaccharide; SNHG15; MiR-362-3p; apoptosis; Oxidative stress; Inflammatory response; INJURY;
D O I
10.14715/cmb/2021.67.6.29
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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-3623pexpression. 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-alpha, 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-alpha, 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-alpha, 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-alpha, 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-miRNC 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-alpha, 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. (C) 2021 by the C.M.B. Association. All rights reserved.
引用
收藏
页码:220 / 227
页数:8
相关论文
共 37 条
  • [1] LncRNA NEAT1 promotes apoptosis and inflammation in LPS-induced sepsis models by targeting miR-590-3p
    Liu, Lingling
    Liu, Fengtao
    Sun, Zhilu
    Peng, Zhengliang
    You, Ting
    Yu, Ziying
    EXPERIMENTAL AND THERAPEUTIC MEDICINE, 2020, 20 (04) : 3290 - 3300
  • [2] MiR-499a suppresses LPS-induced human vascular endothelial cell inflammatory response and apoptosis by regulating STAT1
    Wang, Chunrui
    Zhu, Zhidong
    INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL PATHOLOGY, 2019, 12 (11): : 4232 - 4241
  • [3] Downregulation of miR-486-5p alleviates LPS-induced inflammatory injury, oxidative stress and apoptosis in Chondrogenic cell ATDC5 by targeting NRF1
    Chang, Qing
    Ji, Mingliang
    Li, Chao
    Geng, Rui
    MOLECULAR MEDICINE REPORTS, 2020, 22 (03) : 2123 - 2131
  • [4] CircUSP39/miR-362-3p/TRAF3 Axis Mediates Hypoxia/Reoxygenation-Induced Cardiomyocyte Oxidative Stress, Inflammation, and Apoptosis
    Wang, Jing
    Wang, Xuan
    Cao, Mingying
    Zhang, Lingli
    Lin, Jingna
    INTERNATIONAL HEART JOURNAL, 2023, 64 (02) : 263 - 273
  • [5] SNHG15, a p53-regulated lncRNA, suppresses cisplatin-induced apoptosis and ROS accumulation through the miR-335-3p/ZNF32 axis
    Sun, Yue-Feng
    Wang, Yuan
    Li, Xiao-Dong
    Wang, Hong
    AMERICAN JOURNAL OF CANCER RESEARCH, 2022, 12 (02): : 816 - 828
  • [6] Blocking the REDD1/TXNIP axis ameliorates LPS-induced vascular endothelial cell injury through repressing oxidative stress and apoptosis
    Hou, Xuhui
    Yang, Songhai
    Yin, Jian
    AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 2019, 316 (01): : C104 - C110
  • [7] LncRNA TUG1 reverses LPS-induced cell apoptosis and inflammation of macrophage via targeting MiR-221-3p/SPRED2 axis
    Hu, Lili
    Ye, Hongwei
    Liao, Jianjun
    BIOSCIENCE BIOTECHNOLOGY AND BIOCHEMISTRY, 2020, 84 (12) : 2458 - 2465
  • [8] LncRNA-SNHG16 Protects Against Oxidative Stress-Induced Vascular Endothelial Cell Injury in Cardiovascular Diseases by Regulating the miR-23a-3p-GLS-Glutamine Metabolism Axis
    Wang, Yang
    Zhang, Chengxin
    Liu, Zhuang
    Gao, Xiaotian
    Ge, Shenglin
    APPLIED BIOCHEMISTRY AND BIOTECHNOLOGY, 2025, 197 (02) : 1039 - 1054
  • [9] LncRNA SNHG15 mediates 1-methyl-4-phenylpyridinium (MPP+)-induced neuronal damage through targeting miR-29c-3p/SNCA axis
    Li, Jiazhen
    Sun, Zhaoming
    Song, Lixiang
    NEUROLOGICAL RESEARCH, 2023, 45 (02) : 181 - 190
  • [10] The upregulation of miR-204-3p in LPS-induced acute lung injury aggravated pulmonary endothelial cells apoptosis via targeting sulfatase 2
    Zhang, Liya
    Zhu, Zhengyu
    Zhang, Qian
    Mao, Zhengdao
    ACTA BIOCHIMICA POLONICA, 2021, 68 (02) : 217 - 222