ArticleHereditas2026
Expression of long non-coding RNA NNT-AS1 in children with severe pneumonia and its effect on lipopolysaccharide-induced human embryonic lung fibroblast injury.
Article in Hereditas, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundSevere pneumonia (SP) threatens the quality of life and well-being of children. This study aims to explore the serum NNT-AS1 expression in SP children and its impact on lipopolysaccharide (LPS)-induced injury in human embryonic lung fibroblasts.
methodsThe study included 69 SP children, 62 mild pneumonia (MP) children and 75 healthy controls. A pneumonia cell model was constructed with LPS-induced MRC-5 cells. Loss-of-function experiments were performed using si-NNT-AS1 and miR-23a-3p inhibitor. The NNT-AS1 and miR-23a-3p expression was detected by real-time quantitative polymerase chain reaction. The diagnostic effect and prognostic value of NNT-AS1 were evaluated by receiver operating characteristics curves and Kaplan-Meier method. Cell viability and apoptosis were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry. Inflammatory factors were measured by enzyme-linked immunosorbent assay. The interaction between NNT-AS1 and miR-23a-3p was verified by luciferase reporter gene and RNA immunoprecipitation assays. Pearson correlation coefficient was used to analyze the correlation.
resultsNNT-AS1 was upregulated in SP children and showed good diagnostic efficacy (area under the curve (AUC) = 0.815). High NNT‑AS1 expression predicted a poorer survival. Silencing of NNT-AS1 increased cell viability, decreased apoptosis, and alleviated inflammatory responses. MiR-23a-3p was a target of NNT-AS1. Inhibition of miR-23a-3p partially reversed the protective effects of NNT-AS1 silencing on LPS-induced MRC-5 cell injury.
conclusionsSerum NNT-AS1 is upregulated in SP patients, and its expression is correlated with clinical prognosis. NNT-AS1 participates in LPS-induced cellular damage by regulating miR-23a-3p. These findings provide a new theoretical basis for understanding the pathogenesis of SP.
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