Clinical Diagnostic Value of miR-193a-5p in Neonatal Acute Respiratory Distress Syndrome and Analysis of Its Effect on Human Lung Epithelial Cells.

IF 0.7 4区医学 Q4 PATHOLOGY

Fetal and Pediatric Pathology Pub Date : 2025-03-01 Epub Date: 2025-01-23 DOI:10.1080/15513815.2024.2447579

Chuanrui Zhu, Lun Zhang, Hongfen Ma, Cuicui Zhang, Fang Cheng, Hong An, Wenxiang Zhu

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引用次数: 0

Abstract

Aim: To explore the clinical value of miR-193a-5p in neonatal acute respiratory distress syndrome (ARDS) and its role in ARDS cell model in vitro. Methods: RT-qPCR was utilized to detect miR-193a-5p level. Correlation analysis was implemented to assess the correlation between miR-193a-5p and clinical indicators (IL-6, IL-1β, TNF-α, LUS). Human lung epithelial cells induced by LPS were used to construct ARDS cell model. The effects of miR-193a-5p on cell viability, apoptosis and inflammation were evaluated by CCK-8, flow cytometry and ELISA. The target gene of miR-193a-5p was predicted and verified by StarBaseV2.0 and luciferase reporter gene, respectively. Results: MiR-193a-5p level in the ARDS group was down-regulated. MiR-193a-5p levels were negatively correlated with clinical indicators. In vitro studies revealed that up-regulation of miR-193a-5p significantly improved LPS-induced apoptosis, inflammation and viability inhibition. Conclusion: The expression of miR-193a-5p was decreased in neonatal ARDS, it is negatively correlated with the pro-inflammatory factors levels.

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miR-193a-5p在新生儿急性呼吸窘迫综合征中的临床诊断价值及其对人肺上皮细胞的影响分析

目的：探讨miR-193a-5p在新生儿急性呼吸窘迫综合征（ARDS）中的临床价值及其在体外ARDS细胞模型中的作用。方法：采用RT-qPCR检测miR-193a-5p水平。通过相关分析评估miR-193a-5p与临床指标（IL-6、IL-1β、TNF-α、LUS）的相关性。采用LPS诱导人肺上皮细胞构建ARDS细胞模型。采用CCK-8、流式细胞术和ELISA检测miR-193a-5p对细胞活力、凋亡和炎症的影响。miR-193a-5p的靶基因分别通过StarBaseV2.0和荧光素酶报告基因进行预测和验证。结果：ARDS组MiR-193a-5p水平下调。MiR-193a-5p水平与临床指标呈负相关。体外研究表明，上调miR-193a-5p可显著改善lps诱导的细胞凋亡、炎症和活力抑制。结论：miR-193a-5p在新生儿ARDS中表达降低，与促炎因子水平呈负相关。

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来源期刊

Fetal and Pediatric Pathology 医学-病理学

CiteScore

3.00

自引率

0.00%

发文量

审稿时长

6-12 weeks

期刊介绍： Fetal and Pediatric Pathology is an established bimonthly international journal that publishes data on diseases of the developing embryo, newborns, children, and adolescents. The journal publishes original and review articles and reportable case reports. The expanded scope of the journal encompasses molecular basis of genetic disorders; molecular basis of diseases that lead to implantation failures; molecular basis of abnormal placentation; placentology and molecular basis of habitual abortion; intrauterine development and molecular basis of embryonic death; pathogenisis and etiologic factors involved in sudden infant death syndrome; the underlying molecular basis, and pathogenesis of diseases that lead to morbidity and mortality in newborns; prenatal, perinatal, and pediatric diseases and molecular basis of diseases of childhood including solid tumors and tumors of the hematopoietic system; and experimental and molecular pathology.