医学
呼吸窘迫
肺
呼吸系统
急性呼吸窘迫
人肺
重症监护医学
价值(数学)
病理
内科学
麻醉
机器学习
计算机科学
作者
Chuanrui Zhu,Lun Zhang,Hongfen Ma,Cuicui Zhang,F. Cheng,Hong An,Wenxiang Zhu
标识
DOI:10.1080/15513815.2024.2447579
摘要
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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