血浆miR-1在过敏性鼻炎中下调，并通过靶向BDNF减轻IL-13诱导的鼻上皮炎症

文献信息

中文摘要

背景： 过敏性鼻炎（AR）是一种常见的上呼吸道慢性炎症性疾病，目前缺乏可靠的非侵入性分子生物标志物用于动态疾病监测和治疗指导。本研究旨在评估血浆miR-1在AR中的诊断价值，并探讨其在鼻上皮炎症和氧化应激中的作用及其潜在分子机制。
方法： 通过RT-qPCR对118例AR患者和100例健康对照者的血浆miR-1进行定量，随后与疾病严重程度指标进行相关性分析。采用IL-13刺激的人鼻上皮细胞（HNEpC）模型，在miR-1过表达或敲低后检测细胞活力、凋亡、促炎细胞因子（IL-6、IL-8）和氧化应激标志物（MDA、GSH）。利用生物信息学筛选和双荧光素酶报告基因实验鉴定并验证BDNF为miR-1的直接靶点。通过共转染miR-1模拟物与BDNF过表达载体进行挽救实验。
结果： AR患者血浆miR-1显著降低，并与TNSS和RQLQ评分呈负相关，区分AR与对照的AUC为0.864。在IL-13处理的HNEpC中，miR-1过表达增强细胞活力，减少凋亡，降低IL-6和IL-8分泌，并改善氧化应激（降低MDA，升高GSH）。BDNF被证实为miR-1的直接靶点。BDNF过表达部分逆转了miR-1上调的保护作用。
结论： 血浆miR-1在AR中下调，并与疾病严重程度相关，提示其作为非侵入性诊断生物标志物的潜力。实验证据表明，miR-1可能通过直接靶向BDNF减轻IL-13诱导的HNEpC炎症和氧化应激。

英文摘要

BACKGROUND: Allergic rhinitis (AR), a common chronic inflammatory disorder of the upper airway, currently lacks reliable non-invasive molecular biomarkers for dynamic disease monitoring and therapeutic guidance. This study aimed to evaluate the diagnostic value of plasma miR 1 in AR and to investigate its role in nasal epithelial inflammation and oxidative stress, along with the underlying molecular mechanism.
METHODS: Plasma miR 1 was quantified by RT qPCR in 118 AR patients and 100 healthy controls, followed by correlation analysis with disease severity indices. An IL 13-stimulated human nasal epithelial cell (HNEpC) model was employed to examine viability, apoptosis, pro-inflammatory cytokines (IL 6, IL 8), and oxidative stress markers (MDA, GSH) following miR 1 overexpression or knockdown. Bioinformatic screening and dual-luciferase reporter assays were utilized to identify and validate BDNF as a direct miR 1 target. Rescue experiments were performed through co-transfection of miR 1 mimic with BDNF overexpression vector.
RESULTS: Plasma miR 1 was significantly lower in AR patients and negatively correlated with TNSS and RQLQ scores, yielding an AUC of 0.864 for discriminating AR from controls. In IL 13 treated HNEpC, miR 1 overexpression enhanced cell viability, reduced apoptosis, decreased IL 6 and IL 8 secretion, and ameliorated oxidative stress (lowered MDA, elevated GSH). BDNF was confirmed as a direct target of miR 1. BDNF overexpression partially reversed the protective effects of miR 1 upregulation.
CONCLUSIONS: Plasma miR 1 is downregulated in AR and correlates with disease severity, suggesting its potential as a non invasive diagnostic biomarker. Experimental evidence indicates that miR 1 may alleviate IL 13 induced inflammation and oxidative stress in HNEpC through direct targeting of BDNF.