| 间歇性低氧诱导人脐静脉内皮细胞损伤机制研究 |
| 投稿时间：2017-12-18 修订日期：2018-01-28 点此下载全文 |
| 引用本文：邬春晓,张京春,刘玥,马林沁,乔羽,毛婷,雷舒雁,郑乔仙.间歇性低氧诱导人脐静脉内皮细胞损伤机制研究[J].医学研究杂志,2018,47(11):23-28 |
| DOI：
10.11969/j.issn.1673-548X.2018.11.007 |
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| 基金项目:国家自然科学基金资助项目（81373825、81573817）；国家自然科学基金青年基金资助项目（81403266） |
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| 中文摘要:目的 建立人脐静脉内皮细胞（HUVECs）的间歇性低氧（IH）模型，探讨IH损伤血管内皮细胞的机制。方法 通过低氧气体循环灌注低氧舱，建立HUVECs的IH模型。实验分为正常对照组（CON），间歇性低氧（IH）2、4、6、8、10、12、14、16次循环组，IH+P38 MAPK阻断剂组（INH）以及持续性缺氧组（SH）。采用定量PCR技术（QPCR）检测细胞间黏附因子（intercellular adhesion molecule 1，ICAM-1）、E选择素（E-selectin）、白介素1（interleukin -1， IL-1）、白介素6（interleukin -6，IL-6）、肿瘤坏死因子α（tumor necrosis factor α，TNF-α）基因表达量；Western blot法检测P38 MAPK /NF-κB通路关键靶标蛋白表达量；细胞免疫荧光技术观察NF-κB P65核移位变化，同时检测细胞黏附功能。结果 （1） 与CON组比较，IH刺激下炎性反应相关因子IL-1、IL-6、TNF-α基因表达量升高（P<0.05）。（2） 与CON组比较，IH组HUVECs的p-P38 MAPK蛋白表达水平升高，NF-κB通路靶标蛋白p-IκB、NF-κB P65核蛋白表达水平均升高，而INH组变化不明显。IH组的NF-κB P65出现核移位变化。（3） 细胞黏附实验结果显示IH组人单核细胞系（human acute monocytic leukemia cell line，THP-1）与HUVECs的黏附能力较CON组增强（P<0.05）。结论 IH能够体外诱发HUVECs炎性反应，其机制与激活P38 MAPK/NF-κB信号通路相关。 |
| 中文关键词:间歇性低氧 人脐静脉内皮细胞 P38 MAPK NF-κB |
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| Mechanisms of Intermittent Hypoxia Induced Injury Model of HUVECs |
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| Abstract:Objective To investigate whether IH can cause inflammatory injury in vascular endothelial cells and its underlying mechanism through establishing the intermittent hypoxia induced injury model of HUVECs. Methods HUVECs were treated with cycles of hypoxia/reoxygenation, and they were divided into 4 groups: normal control group (CON group), intermittent hypoxia 2, 4, 6, 8, 10, 12, 14, 16 cycles groups (IH groups), IH + P38 MAPK inhibitor group (INH group) and persistent hypoxia group (SH group). Cellular adhesion function was investigated. Cell adhesion molecules (ICAM-1), E-selectin (E-selectin), interleukin-1 (IL-1), interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α) were detected by inter-quantitative PCR (QPCR). Western-blot was used to measure expression of essential proteins of P38 MAPK/NF-κB pathway. Immunofluorescence was used to detect nuclear translocation of NF-κB P65. Results Inflammatory factor IL-1, IL-6 and TNF-α in IH group was significantly higher than CON group (P<0.05). Also, we detected increased p-P38 MAPK and enchanced nuclear translocation of p-IκB, NF-κB P65, the hallmark proteins of NF-κB pathway, in HUVECs received IH performance. Meanwhile, significant nuclear translocation of NF-κB P65 in IH group was observed. Compared with CON group, HUVECs adhesion capacity of IH group was enhanced (P<0.05). Conclusion In vitro environment, IH causes endothelium inflammation damage through P38 MAPK/NF-κB signaling pathway. |
| keywords:Intermittent hypoxia HUVECs P38 MAPK NF-κB |
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