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

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. 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. 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). 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.