lncRNA NEAT1靶向miR-495-3p对LPS诱导的WI-38细胞损伤的影响

被引：0

作者：

朱曦 ^{[1
]}

郭赟 ^{[2
]}

陆涛 ^{[1
]}

钱俊 ^{[2
]}

机构：

[1] 江南大学附属儿童医院塈无锡市儿童医院重症医学科

[2] 江南大学附属儿童医院塈无锡市儿童医院呼吸内科

来源：

中国免疫学杂志 | 2025年 / 41卷 / 03期

关键词：

lncRNA NEAT1; miR-495-3p; 人胚肺细胞WI-38; 凋亡; 炎症;

D O I：

暂无

中图分类号：

R563.1 [肺炎];

学科分类号：

摘要：

目的：探讨长链非编码RNA(lncRNA)核富集转录体1(NEAT1)通过调控微小RNA-495-3p(miR-495-3p)对脂多糖（LPS）诱导的人胚肺细胞（WI-38）损伤的影响。方法：采用10μg/ml LPS处理WI-38细胞建立体外肺炎模型，采用实时荧光定量聚合酶链式反应（qPCR）检测WI-38细胞中NEAT1和miR-495-3p的表达水平，qPCR检测NEAT1和miR-495-3p的表达。采用双荧光素酶报告基因实验检测NEAT1和miR-495-3p的靶向关系。采用细胞计数试剂盒和流式细胞术分别检测敲低NEAT1对LPS诱导的WI-38细胞增殖活力和凋亡的影响，蛋白质免疫印迹试验检测Bcl-2、Bax和Cleaved caspase-3蛋白质表达。ELISA检测炎症因子IL-6、IL-8和IL-1β的含量。结果：LPS刺激能够上调WI-38中NEAT1的表达，抑制miR-495-3p的表达；双荧光素酶报告基因实验证实NEAT1和miR-495-3p存在靶向关系，且敲低NEAT1能够促进miR-495-3p的表达；LPS能够抑制WI-38细胞增殖促进细胞凋亡，促进炎症因子IL-6、IL-8和IL-1β的表达（P<0.05）；敲低NEAT1能够抑制LPS诱导的WI-38细胞凋亡和炎症反应，促进细胞增殖。结论：敲低NEAT1通过靶向负调控miR-495-3p抑制LPS诱导的WI-38细胞凋亡和炎症反应。

引用

页码：576 / 581

页数：6

共 28 条

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