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ENGLISH ABSTRACT
miR-4508通过PI3K/AKT通路调控温石棉诱导人支气管上皮细胞的炎症反应
王玉君
黄丽
何佳睿
张旭
霍婷婷
董发勤
杨洁
邓建军
作者及单位信息
·
DOI： 10.3760/cma.j.cn112152-20231116-00315
MiR-4508 regulates chrysotile asbestos induced inflammation in human bronchial epithelial cells through the PI3K/AKT pathway
Wang Yujun
Huang Li
He Jiarui
Zhang Xu
Huo Tingting
Dong Faqin
Yang Jie
Deng Jianjun
Authors Info & Affiliations
Wang Yujun
School of Laboratory Medicine, North Sichuan Medical College, Nanchong 637000, China
Huang Li
Department of Clinical Laboratory, Mianyang 404 Hospital, Mianyang 621000, China
He Jiarui
School of Laboratory Medicine, Chengdu Medical College, Chengdu 610500, China
Zhang Xu
Department of Clinical Laboratory, Mianyang 404 Hospital, Mianyang 621000, China
Huo Tingting
School of Environment and Resource, Southwest University of Science and Technology, Mianyang 621010, China
Dong Faqin
School of Environment and Resource, Southwest University of Science and Technology, Mianyang 621010, China
Yang Jie
Department of Clinical Laboratory, Mianyang 404 Hospital, Mianyang 621000, China
Deng Jianjun
School of Laboratory Medicine, North Sichuan Medical College, Nanchong 637000, China
Department of Clinical Laboratory, Mianyang 404 Hospital, Mianyang 621000, China
·
DOI： 10.3760/cma.j.cn112152-20231116-00315
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摘要

目的探讨miR-4508调控温石棉诱导人支气管上皮细胞炎症反应的分子机制。

方法将青海省茫崖市温石棉使用卧式行星仪研磨至超细粉尘，并以人支气管上皮细胞（16HBE细胞）作为染毒细胞，细胞计数试剂盒8法检测细胞存活率，乳酸脱氢酶试剂盒检测细胞毒性，电化学发光技术检测白细胞介素（IL）-6的表达水平，酶联免疫吸附试验检测IL-8的表达水平，实时荧光定量聚合酶链反应筛选并验证miR-4508的表达水平。以AKT抑制剂MK2206作用于16HBE细胞，采用Western blot检测AKT和PTEN的磷酸化水平，利用miR-4508过表达和抑制实验检测AKT和PTEN、IL-6和IL-8蛋白的表达水平。

结果随着温石棉暴露浓度增加，细胞存活率呈一定浓度依赖性下降，乳酸脱氢酶含量逐渐升高。当温石棉暴露浓度≥25 µg/ml时可诱导细胞分泌IL-6和IL-8［温石棉 25、50、75 µg/ml组IL-6的表达水平分别为（325.92±8.61）pg/ml、（331.51±4.96）pg/ml、（378.74±13.77）pg/ml，IL-8的表达水平分别为（94.95±3.11）pg/ml、（357.60±1.80）pg/ml、（537.19±3.11）pg/ml，均高于同组别0 µg/ml组（95.85±1.20）pg/ml和（7.81±0.00）pg/ml，均 P＜0.05］，且IL-8的分泌水平明显高于IL-6。此外，温石棉染毒16HBE细胞后，可诱导miR-4508的高表达，使用MK2206后AKT和PTEN的磷酸化水平降低，IL-6和IL-8表达水平明显降低，并显著降低了miR-4508的表达水平。过表达miR-4508使AKT和PTEN表达水平升高，IL-6和IL-8表达水平明显升高（ P＜0.01）。抑制miR-4508后，AKT和PTEN、IL-6和IL-8表达水平明显降低（ P＜0.01）。

结论青海省茫崖市温石棉可诱导16HBE细胞炎症反应并上调miR-4508的表达水平，上调的miR-4508通过PI3K/AKT信号通路促进温石棉诱导16HBE细胞的炎症反应。

炎症反应;温石棉纤维;miR-4508;PI3K/AKT通路;人支气管上皮细胞
ABSTRACT

ObjectiveTo explore the molecular mechanism of miR-4508 regulating the inflammatory response of human bronchial epithelial cells induced by representative chrysotile asbestos.

MethodsThe chrysotile asbestos was ground into ultrafine dust using a horizontal planetary instrument, and human bronchial epithelium (16HBE) cells were taken as the object of infection. Cell survival rate was detected by cell counting kit-8 method, cytotoxicity was detected by lactate dehydrogenase (LDH) kit. The released of inflammatory factor IL-6 was detected by electrochemical luminescence. The released inflammatory factor IL-8 was detected by enzyme-linked immunosorbent assay. The expression level of miR-4508 was screened and verified by reverse transcription-quantitative real-time polymerase chain reaction. After 16HBE cells were treated with AKT inhibitor MK2206, the phosphorylation levels of AKT and PTEN were detected by western blot. The expression levels of AKT and PTEN and the contents of IL-6 and IL-8 were detected in miR-4508 overexpression and interference experiments.

ResultsWith the increase of chrysotile asbestos exposure concentration, the cell survival rate decreased in a concentration-dependent manner, and the LDH content gradually increased. The secretion of IL-6 and IL-8 in chrysotile 25, 50 and 75 µg/ml groups were (325.92±8.61) pg/ml, (331.51±4.96) pg/ml, (378.74±13.77) pg/ml, and (94.95±3.11) pg/ml, (357.60±1.80) pg/ml, (537.19±3.11) pg/ml, respectively, while the group with 0 µg/ml chrysotile was (95.85±1.20) pg/ml and (7.81±0.00) pg/ml ( P＜0.05). In addition, chrysotile asbestos exposure to 16HBE could induce the high expression of miR-4508 . After pretreatment with MK2206, the phosphorylation levels of AKT and PTEN were decreased, the contents of IL-6 and IL-8 were significantly decreased, and the expression level of miR-4508 was significantly reduced. Overexpression of miR-4508 significantly increased the expressions of AKT and PTEN, and the contents of IL-6 and IL-8 ( P＜0.01). After interfering with miR-4508, the expressions of AKT and PTEN were significantly decreased, and the contents of IL-6 and IL-8 were significantly decreased ( P＜0.01).

ConclusionsChrysotile asbestos can induce the inflammatory response of 16HBE cells and up-regulate the expression level of miR-4508. The up-regulation of miR-4508 promotes the 16HBE inflammatory response induced by chrysotile asbestos through the PI3K/AKT pathway.

Inflammatory response;Chrysotile asbestos;MiR-4508;PI3K/AKT pathway;Human bronchial epithelial cells
Deng Jianjun, Email: mocdef.3ab611080gnednujnaij
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引用本文

王玉君,黄丽,何佳睿,等. miR-4508通过PI3K/AKT通路调控温石棉诱导人支气管上皮细胞的炎症反应[J]. 中华肿瘤杂志,2025,47(03)：244-253.

DOI:10.3760/cma.j.cn112152-20231116-00315

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温石棉是一种性能优良且价格低廉的矿物纤维材料，广泛应用于建筑、化工及国防等众多领域。我国是全球温石棉最大消费国和第二大生产商，全国超过100万人有职业暴露 ［ 1 , 2 ］ 。研究显示，温石棉暴露引起的石棉肺与肺癌的发生有关 ［ 3 ］ ，包括恶性间皮瘤在内的所有胸膜癌与首次暴露温石棉的时间成正比 ［ 4 ］ 。前期研究显示，温石棉主要由二氧化硅、氧化镁及少量的三氧化二铁、二氧化铝和铬、镍等微量元素组成 ［ 5 ］ ，因矿床地理环境因素不同而表现出不同的细胞毒性 ［ 6 ］ ，其诱导肺部疾病的机制包括氧化应激、慢性炎症、DNA 损伤和基因调控等多个方面 ［ 7 , 8 , 9 ］ 。其中，炎症反应是机体重要的一种免疫防御机制，涉及多个信号通路的激活，包括核因子κB、PI3K/AKT和NLRP3/caspase-1 ［ 10 , 11 ］ 。miRNA是一种只有18～25个碱基的非编码RNA，参与转录后水平的调控，可与mRNA的3'UTR区域互补序列共价结合，从而抑制翻译。研究证明，miRNA控制着许多细胞过程，如增殖、分化和细胞死亡 ［ 12 ］ 。Hiraku等 ［ 13 ］ 发现miR-21在石棉暴露的动物肺组织中表达升高，同时抑癌基因表达下调，miR-21上调是石棉暴露的早期事件，可能导致肺毒性和致癌。目前，miRNA在温石棉诱导支气管上皮细胞毒性的调控作用研究甚少，本研究采用人支气管上皮细胞（16HBE细胞）作为染毒对象，探讨miR-4508调控温石棉诱导16HBE细胞炎症反应的分子机制，以期为筛选温石棉致肺部疾病的早期分子标志物提供理论依据。
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邓建军，Email： mocdef.3ab611080gnednujnaij
B

王玉君：酝酿和设计实验、实验研究、采集数据、起草文章；黄丽：实验研究、采集数据、分析/解释数据；何佳睿：实验研究、采集数据；张旭：分析/解释数据、统计学分析、对文章的知识性内容批评性审阅；霍婷婷：行政、技术和材料支持、对文章的知识性内容批评性审阅；董发勤：行政、技术和材料支持、对文章的知识性内容批评性审阅；杨洁：获取研究经费、论文修改；邓建军：对文章的知识性内容批评性审阅、获取研究经费、论文修改、行政、技术和材料支持、指导

C
本研究得到了西南科技大学彭同江教授及课题组赵丁冉对实验操作的指导和帮助
D
王玉君, 黄丽, 何佳睿, 等. miR-4508通过PI3K/AKT通路调控温石棉诱导人支气管上皮细胞的炎症反应[J]. 中华肿瘤杂志, 2025, 47(3): 244-253. DOI: 10.3760/cma.j.cn112152-20231116-00315.
E
所有作者声明无利益冲突
F
四川省医学会科研课题 (S20029)
四川省自然科学基金项目面上项目 (2023NSFSC0650)
四川省医学青年创新科研课题计划 (Q23073)
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