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Background <p>Chronic obstructive pulmonary disease (COPD) is a respiratory disease with complex causes; its pathogenesis remains unclear. This study explores the regulatory relationship between NORAD and miR-150-5p to provide novel insights for COPD treatment.</p> Methods <p>Serum from 108 COPD patients and 94 healthy controls were collected. qPCR measured NORAD and miR-150-5p expression, while dual-luciferase assays verified their interaction. The clinical relevance of NORAD was analyzed using ROC, logistic, and Pearson methods. Human pulmonary microvascular endothelial cells (hPMECs) were treated with 5% cigarette smoke extract (CSE) for 36&#xa0;h to establish a cell injury model. NORAD was silenced alone or co-inhibited with miR-150-5p in this model. Inflammatory and oxidative stress markers were measured by ELISA, and cell proliferation was assessed using the CCK-8 assay.</p> Results <p>COPD patients exhibited significantly elevated serum NORAD level (<i>P</i> &lt; 0.001), with higher levels in acute exacerbation than stable phases (<i>P</i> &lt; 0.001). NORAD showed high diagnostic (AUC = 0.867, <i>P</i> &lt; 0.001) and predictive value (OR = 3.271, <i>P</i> = 0.002) for COPD and was significantly correlated with lung function (<i>P</i> &lt; 0.05). Serum NORAD was strongly negatively correlated with miR-150-5p (<i>r </i>= -0.749, <i>P</i> &lt; 0.001), indicating a targeted regulatory relationship (<i>P</i> &lt; 0.001). After CSE treatment, NORAD expression in hPMECs was significantly up-regulated (<i>P</i> &lt; 0.001). NORAD knockdown reduced inflammation (<i>P</i> &lt; 0.001), oxidative stress (<i>P</i> &lt; 0.01), and reversed CSE-induced proliferation inhibition (<i>P</i> &lt; 0.001). Co-inhibition of NORAD and miR-150-5p reversed the protective effect of NORAD knockdown (<i>P</i> &lt; 0.05).</p> Conclusion <p>NORAD can regulate miR-150-5p, and both NORAD and miR-150-5p may serve as potential therapeutic targets for COPD, offering a promising strategy for modulating disease progression.</p>

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Clinical significance of LncRNA NORAD and its potential mechanism in chronic obstructive pulmonary disease

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月14日

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  • Linjuan Su,
  • Bing Liang

摘要

Background

Chronic obstructive pulmonary disease (COPD) is a respiratory disease with complex causes; its pathogenesis remains unclear. This study explores the regulatory relationship between NORAD and miR-150-5p to provide novel insights for COPD treatment.

Methods

Serum from 108 COPD patients and 94 healthy controls were collected. qPCR measured NORAD and miR-150-5p expression, while dual-luciferase assays verified their interaction. The clinical relevance of NORAD was analyzed using ROC, logistic, and Pearson methods. Human pulmonary microvascular endothelial cells (hPMECs) were treated with 5% cigarette smoke extract (CSE) for 36 h to establish a cell injury model. NORAD was silenced alone or co-inhibited with miR-150-5p in this model. Inflammatory and oxidative stress markers were measured by ELISA, and cell proliferation was assessed using the CCK-8 assay.

Results

COPD patients exhibited significantly elevated serum NORAD level (P < 0.001), with higher levels in acute exacerbation than stable phases (P < 0.001). NORAD showed high diagnostic (AUC = 0.867, P < 0.001) and predictive value (OR = 3.271, P = 0.002) for COPD and was significantly correlated with lung function (P < 0.05). Serum NORAD was strongly negatively correlated with miR-150-5p (r = -0.749, P < 0.001), indicating a targeted regulatory relationship (P < 0.001). After CSE treatment, NORAD expression in hPMECs was significantly up-regulated (P < 0.001). NORAD knockdown reduced inflammation (P < 0.001), oxidative stress (P < 0.01), and reversed CSE-induced proliferation inhibition (P < 0.001). Co-inhibition of NORAD and miR-150-5p reversed the protective effect of NORAD knockdown (P < 0.05).

Conclusion

NORAD can regulate miR-150-5p, and both NORAD and miR-150-5p may serve as potential therapeutic targets for COPD, offering a promising strategy for modulating disease progression.