Objective To investigate the correlation between the activation of peripheral blood neutrophil extracellular traps (NETs), oxidative stress levels, and the risk of developing acute respiratory distress syndrome (ARDS) in patients with multiple trauma, thereby providing a basis for the early prediction and intervention of post-traumatic ARDS. Methods This prospective cohort study enrolled 168 patients with multiple trauma admitted to our hospital between February 2023 and September 2025. Peripheral venous blood was collected within 24 hours of admission and on day 3 after treatment initiation. Plasma levels of NETs markers [neutrophil elastase (NE), citrullinated histone H3 (CitH3), myeloperoxidase (MPO)] and oxidative stress indicators [malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx)] were measured. All patients were followed for 28 days post-admission and were categorized into ARDS and non-ARDS groups based on ARDS occurrence during follow-up. Univariate analysis, multivariate logistic regression analysis, and receiver operating characteristic (ROC) curve analysis were used to assess the correlation and predictive value of NETs and oxidative stress levels for ARDS risk. Results All 168 patients completed the 28-day follow-up. During follow-up, 42 patients (25.0%) developed ARDS. The ARDS group had significantly higher ISS scores, longer mechanical ventilation duration, and a higher proportion of surgical interventions, but lower Glasgow Coma Scale (GCS) scores at admission compared to the non-ARDS group (all P<0.05). At both 24 hours post-admission and on day 3 post-treatment, the ARDS group exhibited significantly higher levels of NE, CitH3, MPO, and MDA, and significantly lower levels of SOD and GPx compared to the non-ARDS group (all P<0.05). By day 3 post-treatment, levels of the aforementioned NETs markers and MDA had decreased, while SOD and GPx levels had increased in both groups; however, the magnitude of improvement was significantly smaller in the ARDS group (all P<0.05). Repeated measures ANOVA revealed statistically significant "time × group" interaction effects for NE, CitH3, MPO, MDA, SOD, and GPx levels (all P<0.05). Multivariate logistic regression analysis identified higher levels of NE, CitH3, MPO, and MDA at 24 hours post-admission as independent risk factors for ARDS, while higher levels of SOD and GPx at the same timepoint were independent protective factors (P<0.05). ROC analysis showed that the combination of plasma NE, CitH3, MPO, MDA, SOD, and GPx levels at 24 hours post-admission predicted ARDS risk with an AUC of 0.811 (95%CI: 0.728-0.895), which was significantly superior to the predictive efficacy of any single indicator alone (Z=3.344, 3.391, 3.069, 2.208, 2.794, 2.021, respectively; all P<0.05). Conclusion Enhanced peripheral blood NETs activation and oxidative stress imbalance are closely associated with an increased risk of ARDS in patients with multiple trauma. NE, CitH3, MPO, MDA, SOD, GPx are independent influencing factors for ARDS risk. Combined dynamic monitoring of these indicators can effectively enhance the predictive power for ARDS risk.
Objective To investigate the molecular mechanisms by which the long non-coding RNA (lncRNA) MIR223HG affects the proliferation, migration and apoptosis of lung adenocarcinoma cells. MethodsDNA damaging agent Zeocin was used to treat human embryo lung cell (MRC-5) and lung cancer cell (A549 and H1299), and the expression of MIR223HG was tested by quantitative real-time polymerase chain reaction (qRT-PCR) analysis. Moreover, the ataxia-telangiectasia mutated (ATM) protein and ATM pathway downstream factor Cell cycle checkpoint kinase 2 (Chk2), p53 tumor suppressor protein (p53) in the lung cancer cell (A549 and H1299) with Zeocin were also tested by qRT-PCR. Cell transfection and Transwell migration assay, colony formation assays, apoptosis assays were performed to verify the role of ATM in the expression of MIR223HG in lung adenocarcinoma. ResultsThe expression of MIR223HG was reduced markedly in the lung cancer cells (A549 and H1299) compared with human embryo lung cell (MRC-5) after treated with Zeocin. ATM protein and its downstream factors Chk2, p53 involved in the process, and ATM regulated the expression of MIR223HG in the lung cancer cells with Zeocin. Futhermore, ATM joined in the processes that MIR223HG regulated the lung cancer cells proliferation, migration and apoptosis. Conclusions The expression of MIR223HG is related to the DNA damage response in the lung cancer, and MIR223HG regulates lung cancer cells proliferation, migration and apoptosis by ATM/Chk2/p53 pathway. MIR223HG may be a potential therapeutic target for lung adenocarcinoma treatment.