Diagnostic value of miR-6510-3p in sepsis-induced acute lung injury and its mechanism targeting ACTB

Abstract Background Sepsis is a systemic inflammatory response triggered by infection and represents one of the common causes of acute lung injury (ALI). Aim To evaluate the clinical diagnostic value of miR-6510-3p in sepsis-induced acute lung injury and its mechanism of action targeting ACTB. Materials and methods Receiver Operating Characteristic (ROC) curves were performed to assess the miR-6510-3p diagnostic value. The cell viability was determined using the CCK-8 kit. Inflammatory factors were evaluated using an ELISA kit. The oxidative stress markers were measured using the Reactive Oxygen Species (ROS) kit, malondialdehyde (MDA) kit and glutathione (GSH) detection kit, respectively. Dual luciferase assays, RNA immunoprecipitation (RIP) experiments, and Spearman correlation analyses were employed to evaluate the target relationship between miR-6510-3p and ACTB. Results miR-6510-3p was down-regulated in plasma samples from both non-ALI sepsis patients and sepsis-induced ALI patients, exhibiting the most pronounced decrease‌ in the latter group, whereas ACTB expression showed an opposite trend. The ROC curve for miR-6510-3p not only distinguishes healthy individuals from non-ALI sepsis patients but also effectively differentiates non-ALI sepsis patients from sepsis-induced ALI patients. Overexpression of miR-6510-3p reduced the release of inflammatory cytokines (TNF-α and IL-6), oxidative stress markers (ROS, MDA and GSH), and the occurrence of apoptosis in LPS-induced HPMECs, promoting the restoration of cell viability and VE-cadherin expression. However, these effects could be reversed by ACTB overexpression. Conclusion miR-6510-3p exhibited high diagnostic value for sepsis-induced ALI and alleviated inflammation, oxidative stress, and apoptosis in LPS-induced HPMECs by regulating ACTB.