Hereditas · 2026
Expression of long non-coding RNA NNT-AS1 in children with severe pneumonia and its effect on lipopolysaccharide-induced human embryonic lung fibroblast injury.
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Jian Fanghua, Fu Jun, Li Dan, Bao Weiqiang
Аннотация
BACKGROUND: Severe 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.
METHODS: The 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.
RESULTS: NNT-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.
CONCLUSIONS: Serum 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.
METHODS: The 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.
RESULTS: NNT-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.
CONCLUSIONS: Serum 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.