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Chronic airway inflammation induced by cigarette smoke (CS) plays an essential role in the pathogenesis of chronic obstructive pulmonary disease (COPD). MALAT1 is involved in a variety of inflammatory disorders. However, studies focusing on the interaction between MALAT1 and CS-induced airway inflammation remain unknown. The present study investigated the effects and mechanisms of MALAT1 in CS-induced airway inflammation in the pathogenesis of COPD. RT-qPCR was employed to determine the mRNA levels of MALAT1, miR-30a-5p and inflammatory cytokines. Protein concentrations of IL-1β and IL-6 in cell culture supernatant and mouse bronchoalveolar lavage fluid (BALF) were assessed by ELISA assay kits. Dual-luciferase reporter assay was conducted to verify the interaction between MALAT1 and miR-30a-5p. The protein expression of JNK and p-JNK was determined by western blot (WB). MALAT1 was highly expressed in cigarette smoke extract (CSE)-treated human bronchial epithelial cells (HBECs) and COPD mice lung tissues. Knockdown of MALAT1 significantly alleviate CS-induced inflammatory response. MALAT1 directly interacted with miR-30a-5p and knockdown of miR-30a-5p significantly inhibit the protective effects of MALAT1 silencing after CS exposure. Additionally, our results showed that miR-30a-5p could regulate inflammation via modulating the activation of JNK signaling pathway. Moreover, our results demonstrated MALAT1 could activate JNK signaling pathway by sponging miR-30a-5p. Our results demonstrated MALAT1 promotes CS-induced airway inflammation by inhibiting the activation of JNK signaling pathway via sponging miR-30a-5p., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier B.V.)

Neuroinflammation and oxidative stress induced by intermittent hypoxia (IH) are associated with cognitive dysfunction in patients with obstructive sleep apnea (OSA). Recently, TAR DNA-binding protein 43 (TDP-43), histone deacetylase 6 (HDAC6), and peroxiredoxin 1 (Prdx1) have been reported to be involved in cognitive impairment in many degenerative diseases; however, the underlying mechanisms remain unclear. In the present study, subjects underwent polysomnography to diagnose OSA. Cognitive function was evaluated using the Montreal Cognitive Assessment (MoCA) and peripheral blood samples were collected. HMC3 cells were treated with lipopolysaccharide (LPS) to mimic in vitro neuroinflammation. Western blotting was used to assess protein expression and ELISA to assess inflammation and oxidative stress levels. Participants were divided into three groups: healthy control (n = 20); mild to moderate OSA (n = 20); and severe OSA (n = 20). The MoCA scores in mild-moderate OSA and severe OSA were lower than those in healthy controls. Continuous positive airway pressure therapy was found to be effective for cognitive impairment in subjects with severe OSA (24.70 ± 1.81). Expression of TDP-43 and HDAC6 was increased in subjects with OSA, whereas Prdx1 expression was decreased. Alterations in these proteins were partially reversed after 12 weeks of CPAP treatment. Protein expression of TDP-43 and HDAC6 was negatively correlated with MoCA scores in patients with OSA, while Prdx1 expression exhibited the opposite trend. In LPS-treated HMC3 cells, TDP-43 and HDAC6 were upregulated, whereas Prdx1 expression was reduced. TDP-43 influenced the expression of Prdx1 by regulating HDAC6, and inflammation and oxidative stress varied with the expression of TDP-43. When a specific inhibitor of HDAC6 was used, LPS-induced inflammation and oxidative stress were alleviated by an elevated level of Prdx1. In summary, findings of the present study suggest that TDP-43 influenced Prdx1 by regulating HDAC6 expression and promoting neuroinflammation and oxidative stress. This process may be involved in the cognitive impairment experienced by patients with OSA and may provide potential therapeutic targets., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023. Published by Elsevier B.V.)

Chronic obstructive pulmonary disease (COPD) is a significant cause of morbidity and mortality worldwide and is characterized by chronic airway inflammation and lung parenchymal cell apoptosis. Cigarette smoke is the major risk factor for the occurrence and development of COPD. Taxifolin (TAX) showed promising pharmacological effects in the management of inflammation, oxidative stress, and apoptosis. In the present study, our results demonstrated that TAX significantly alleviated cigarette smoke-induced inflammation and apoptosis both in vivo and in vitro. TAX notably lowered the elevated total cell count in mouse BALF compared with that in the COPD group. The cigarette smoke-induced emphysematous changes were remarkably reversed by TAX. In addition, treatment with TAX suppressed the elevated mRNA and protein levels of IL-1β, IL-6 and TNF-α in COPD mouse lung tissue and cigarette smoke extract (CSE)-treated human bronchial epithelial cells (HBECs). Additionally, TAX significantly decreased the ratios of p-iκB to iκB and p-p65 to p65 compared with the COPD group and CSE-treated HBECs. Moreover, the results of the TUNEL assay and flow cytometry also demonstrated the anti-apoptotic effect of TAX in mouse lung tissue and HBECs. Furthermore, the elevated Bax and CCP3 levels and decreased Bcl-2 levels induced by cigarette smoke were significantly reversed by TAX treatment in vivo and in vitro. Our results highlight the ameliorating effects of TAX against cigarette smoke-induced inflammation and apoptosis in the pathogenesis of COPD., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022. Published by Elsevier B.V.)

Emerging studies have noted that dysregulated long non-coding RNAs (lncRNAs) are implicated in the pathological processes of chronic obstructive pulmonary disease (COPD). LncRNA colon cancer-associated transcript 1 (CCAT1) plays well-defined roles in the inflammatory progression. The study aims to figure out the effect and regulatory mechanism of CCAT1 in the cigarette smoke induced inflammation in COPD. The results showed that CCAT1 was highly expressed in lung tissues of smokers with COPD compared with never-smokers without COPD. In human bronchial epithelial (HBE) cells, cigarette smoke extract (CSE) treatment led to an increase in CCAT1 expression in a dose- and time- dependent manner. Functional experiments showed that knockdown of CCAT1 amelioratedCSE-inducedinflammation. Mechanistically, CCAT1 directly targeted miR-152-3p, and miR-152-3p overexpression reversed the pro-inflammatory effects of CCAT1 on HBE cells. Subsequently, miR-152-3p was found to regulate ERK signaling pathway. PD98059, an ERK specific inhibitor, reversed miR-152-3p knockdown mediated inflammation in HBE cells. In addition, CCAT1 acted as a sponge for miR-152-3p to positively regulate ERK signaling pathway. Overall, current findings suggest that CCAT1 promoted inflammation by activating ERK signal pathway via sponging miR-152-3p in CSE-treated HBE cells. These results may provide a novel therapeutic target for alleviating cigarette smoke mediated airway inflammation., (Copyright © 2022 Elsevier B.V. All rights reserved.)