miR-199a-5p缓解辐射诱导的人脐静脉内皮细胞系细胞损伤

doi:10.16352/j.issn.1001-6325.2026.11.1455

基础医学与临床 ›› 2026, Vol. 46 ›› Issue (11): 1455-1462.doi: 10.16352/j.issn.1001-6325.2026.11.1455

miR-199a-5p缓解辐射诱导的人脐静脉内皮细胞系细胞损伤

刘晨曦¹, 文雯¹, 屈明玥², 靳志涛³, 陆晓炯⁴, 许娇娇³, 张铮^1*

中国人民解放军火箭军特色医学中心 1.职业病治疗科;2.研究部;3.心血管内科;4.呼吸内科,北京 100088

收稿日期:2025-10-29 修回日期:2026-01-26 出版日期:2026-11-05 发布日期:2026-10-26
通讯作者: ^*Faithword@163.com
基金资助:
北京市自然科学基金(7222229)

miR-199a-5p alleviates irradiation-induced injury in human umbilical vein endothelial cell line

LIU Chenxi¹, WEN Wen¹, QU Mingyue², JIN Zhitao³, LU Xiaojiong⁴, XU Jiaojiao³, ZHANG Zheng^1*

1. Department of Occupational Disease Treatment; 2. Research Department; 3. Department of Cardiology; 4. Department of Respiratory Medicine, Chinese People′s Liberation Army Rocket Force Characteristic Medical Center, Beijing 100088, China

Received:2025-10-29 Revised:2026-01-26 Online:2026-11-05 Published:2026-10-26
Contact: ^*Faithword@163.com

摘要/Abstract

摘要： 目的探讨miR-199a-5p对辐射诱导人脐静脉内皮细胞(HUVECs)损伤的作用及其可能机制。方法用不同剂量(3、6、9、12 Gy)X射线对HUVECs进行照射。分别通过CCK-8法、annexin V/PI双染法和二氢乙啶(DHE)荧光探针检测细胞活力、凋亡率和活性氧(ROS)水平,以确定构建辐射损伤细胞模型的最佳剂量。随后,将HUVECs分为对照组(Ctrl)、辐射组(Ir)、辐射 + 转染阴性对照组(Ir+NC)、辐射 + miR-199a-5p模拟物组(Ir+miR-199a-5p),评估miR-199a-5p对细胞凋亡和ROS水平的影响。进一步采用MitoSOX^TM Red探针及JC-1探针检测线粒体超氧化物-与线粒体膜电位(ΔΨm)。结果 9 Gy X射线照射可显著降低HUVECs活性(P＜0.05)、诱导细胞凋亡并升高胞内ROS水平(P＜0.05)。miR-199a-5p能够显著减少辐射诱导的HUVECs凋亡及氧化应激水平(P＜0.05)。与此同时,miR-199a-5p可显著抑制辐射诱导的线粒体超氧化物生成(P＜0.05),并稳定线粒体膜电位。结论 miR-199a-5p可能通过抑制线粒体氧化应激并稳定线粒体膜电位,减轻辐射诱导的HUVECs损伤。

关键词: miR-199a-5p, 辐射损伤, 线粒体, 氧化应激, 凋亡

Abstract: Objective To investigate the protective effect of miR-199a-5p on irradiation-induced injury in human umbilical vein endothelial cells (HUVECs) as well as underlying mechanism. Methods In order to determine the optimal irradiation dose for establishing the injury model.HUVECs were irradiated with X-rays of varying doses (3, 6, 9, and 12 Gy). Cell viability was assessed by CCK-8 assay. Apoptosis was examined by annexin V/PI double staining. The level of intracellular reactive oxygen species (ROS) was evaluated by dithydroethidium (DHE) fluorescent probe. The cells were divided into following four groups as control (Ctrl), irradiation alone (Ir), irradiation + negative control transfection (Ir+NC), and irradiation + miR-199a-5p mimic (Ir+miR-199a-5p). The effects of miR-199a-5p on apoptosis and ROS level were examined. Mitochondrial super oxide production and mitochondrial membrane potential (ΔΨm) were measured by MitoSOX^TM Red and JC-1 probes, respectively. Results Irradiation at 9 Gy significantly suppressed HUVECs viability (P＜0.05),induced apoptosis and enhanced intracellular ROS level(P＜0.05). Over-expression of miR-199a-5p markedly attenuated irradiation-induced apoptosis and oxidative stress (P＜0.05). Furthermore, miR-199a-5p effectively suppressed mitochondrial super oxide generation (P＜0.05) and maintained mitochondrial membrane potential stability after irradiation. Conclusions miR-199a-5p may alleviate irradiation-induced HUVECs injury by inhibiting mitochondrial oxidative stress and stabilizing mitochondrial membrane potential.

Key words: miR-199a-5p, irradiation injury, mitochondrial, oxidative stress, apoptosis

中图分类号:

R541.9

刘晨曦, 文雯, 屈明玥, 靳志涛, 陆晓炯, 许娇娇, 张铮. miR-199a-5p缓解辐射诱导的人脐静脉内皮细胞系细胞损伤[J]. 基础医学与临床, 2026, 46(11): 1455-1462.

LIU Chenxi, WEN Wen, QU Mingyue, JIN Zhitao, LU Xiaojiong, XU Jiaojiao, ZHANG Zheng. miR-199a-5p alleviates irradiation-induced injury in human umbilical vein endothelial cell line[J]. Basic & Clinical Medicine, 2026, 46(11): 1455-1462.

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miR-199a-5p缓解辐射诱导的人脐静脉内皮细胞系细胞损伤

miR-199a-5p alleviates irradiation-induced injury in human umbilical vein endothelial cell line

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