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

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.