| 王静,邵小美,盛娜,杨震.沉默lncRNA NEAT1通过抑制NF-κB通路减轻LPS 诱导的支气管上皮细胞炎症反应.[J].中南医学科学杂志.,2023,(5):655-659. |
| 沉默lncRNA NEAT1通过抑制NF-κB通路减轻LPS 诱导的支气管上皮细胞炎症反应 |
| Silencing lncRNA NEAT1 alleviates LPS-induced inflammation of bronchial epithelial cells by inhibiting NF-κ B pathway |
| 投稿时间：2022-12-23 修订日期：2023-07-29 |
| DOI：10.15972/j.cnki.43-1509/r.2023.05.007 |
| 中文关键词: 长链非编码RNA 核因子-κB通路 脂多糖 支气管上皮细胞 炎症反应 [ |
| 英文关键词:lncRNA NF-κB LPS bronchial epithelial cells inflammatory response |
| 基金项目:南京市卫生科技发展专项资金项目(ykk18240) |
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| 中文摘要: |
| 目的探究沉默长链非编码RNA(lncRNA)NEAT1对脂多糖(LPS)诱导的人支气管上皮(HBE)细胞(16HBE)炎症反应的影响及机制。 方法16HBE细胞分为Control组、LPS组、LPS+si-NC组和LPS+si-NEAT1组。实时荧光定量PCR检测各组lncRNA NEAT1、白细胞介素(IL)-1β、IL-6及肿瘤坏死因子-α(TNF-α)的mRNA表达水平；MTT法检测细胞增殖活力；流式细胞仪检测细胞凋亡率；Western blotting检测各组炎症因子水平及增殖细胞核抗原(PCNA)、p53、核因子κB抑制蛋白(IκB)α、核因子-κB(NF-κB)p65蛋白表达水平。 结果沉默lncRNA NEAT1后,IL-1β、IL-6、TNF-α及其mRNA表达水平、细胞凋亡率及p53、p-IκBα、p-NF-κB p65蛋白水平均明显降低,细胞增殖活力及PCNA蛋白水平均明显升高(P＜0.05),细胞中p-NF-κB p65相对荧光强度(细胞核/细胞质)降低(P＜0.05)。 结论沉默lncRNA NEAT1表达抑制16HBE细胞炎症反应,其机制可能与抑制NF-κB通路的激活有关。 |
| 英文摘要: |
| AimTo study the effect of silencing long non-coding RNA (lncRNA) NEAT1 on lipopolysaccharide (LPS)-induced inflammatory response in human bronchial epithelial cells (16HBE) and to discuss its underlying mechanism. Methods16HBE cells were divided into Control group, LPS group, LPS+si-NC group, and LPS+si-NEAT1 group. Quantitative real-time PCR was used to detect the mRNA expression levels of lncRNA NEAT1, interleukin-1β (IL-1β), IL-6 and tumor necrosis factor-α (TNF-α) in each group of 16HBE cells; MTT assay was used to detect cell proliferation activity; Flow cytometry was used to detect cell apoptosis rate; Western blotting was used to detect the levels of inflammatory factors, protein expression levels of proliferating cell nuclear antigen (PCNA), apoptosis regulatory gene p53, inhibitor of nuclear factor κB (IκB) α and nuclear factor-κB (NF-κB) p65 in each group of 16HBE cells. ResultsAfter silencing the expression level of lncRNA NEAT1, the mRNA expression levels and proteins of IL-1β, IL-6, and TNF-α, as well as the apoptosis rate and the protein levels of p53, p-IκBα, p-NF-κB p65 in 16HBE cells were significantly reduced. The cell proliferation activity and PCNA protein level were significantly increased (P＜0.05). The relative fluorescence intensity (nucleus/cytoplasm) of p-NF-κB p65 was decreased (P＜0.05). ConclusionDown-regulating the expression of lncRNA NEAT1 can reduce the inflammatory response and inhibit the activation of the NF-κB pathway. |
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