Evidence map›Paper›PMID 41801306›Full record

ArticleLung2026

Mechanisms of Anti-Oxidants, N-Acetylcysteine and Elamipretide (SS-31), on Ozone-Induced Airway Hyperresponsiveness and Mucus Hypersecretion.

Meiqin Xie, Jiali Weng, Chenfei Li, Qi Liu, Yi Feng, Hai Zhang, Qing Chang, Kian Fan Chung, Ian M Adcock, Feng Li and 1 more

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Article in Lung, 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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1 · What the graph read from it

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

11 authors.

Meiqin Xie *Department of Geriatric Respiratory and Critical Care Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, People's Republic of China.
Jiali Weng *Department of Pulmonary and Critical Care Medicine, Shanghai Chest Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200030, People's Republic of China.
Chenfei LiDepartment of Pulmonary and Critical Care Medicine, Shanghai Chest Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200030, People's Republic of China.
Qi LiuDepartment of Pulmonary and Critical Care Medicine, Shanghai Chest Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200030, People's Republic of China.
Yi FengDepartment of Pulmonary and Critical Care Medicine, Shanghai Chest Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200030, People's Republic of China.
Hai ZhangDepartment of Pulmonary and Critical Care Medicine, Shanghai Chest Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200030, People's Republic of China.
Qing ChangDepartment of Pulmonary and Critical Care Medicine, Shanghai Chest Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200030, People's Republic of China.
Kian Fan ChungAirway Disease Section, National Heart and Lung Institute, Imperial College, Dovehouse Street, London, SW3 6LY, UK.
Ian M AdcockAirway Disease Section, National Heart and Lung Institute, Imperial College, Dovehouse Street, London, SW3 6LY, UK.
Feng LiDepartment of Pulmonary and Critical Care Medicine, Shanghai Chest Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200030, People's Republic of China. lifeng741@aliyun.com.
Xiaoyun FanDepartment of Geriatric Respiratory and Critical Care Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, People's Republic of China. xiaoyunfan@ahmu.edu.cn.

Funding

Anhui Provincial Institute of Translational Medicine 202304295107020044National Natural Science Foundation of China 81870031National Natural Science Foundation of China U1803126Shanghai Jiao Tong University YG2019ZDA24
6 · The paper itself

Abstract

backgroundOzone (O₃) exposure induces acute airway injury characterized by airway hyperresponsiveness (AHR) and airway mucus hypersecretion (AMH). Oxidative stress and mitochondria-derived reactive oxygen species (mtROS) are key contributors. We investigated and compared the protective mechanisms of N-acetylcysteine (NAC) and the mitochondria-targeted antioxidant Elamipretide (SS-31) in O₃-induced airway inflammation, AHR and AMH.

methodsWild-type C57BL/6J mice received intraperitoneal NAC or SS-31 1 h before a single O₃ exposure. AHR, bronchoalveolar lavage (BAL) inflammatory cells, mucus production and mucin expression, inflammatory mediators, oxidative stress indices, and PI3K/AKT and NLRP3/caspase-1/GSDMD pathway activation were assessed in vivo. BEAS-2B cells were pretreated with NAC, SS-31, or the PI3K/AKT inhibitor LY294002 before O₃ exposure, and pathway activation was evaluate d in vitro.

resultsNAC and SS-31 comparably attenuated O₃-induced AHR, reduced BAL inflammatory cell influx, and decreased AMH and MUC5B expression. Both treatments improved redox balance by reducing ROS/mtROS, lowering malondialdehyde (MDA), increasing superoxide dismutase (SOD) activity, and improving GSH/GSSG. NAC and SS-31 also suppressed O₃-induced inflammatory gene expression and inhibited activation of PI3K/AKT and NLRP3/caspase-1/GSDMD signaling in mouse lungs and BEAS-2B cells. PI3K inhibition recapitulated these protective effects in vitro, supporting a mechanistic role for PI3K/AKT signaling during acute O₃ exposure.

conclusionsNAC and SS-31 protect against acute O₃-induced AHR and AMH by alleviating oxidative stress and suppressing PI3K/AKT-driven inflammatory and pyroptotic pathways. Targeting oxidative stress, including mitochondrial ROS, may represent a viable strategy to mitigate airway damage caused by acute O₃ exposure.

Indexed as

AcetylcysteineAntioxidantsBronchial HyperreactivityLungMucusOligopeptidesAnimalsBronchoalveolar Lavage FluidCaspase 1Cell LineDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLMitochondriaAcetylcysteineAntioxidantsCaspase 1elamipretideNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseOligopeptidesOzonePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesAirway hyperresponsivenessAirway mucus hypersecretionAntioxidantsMitochondriaOxidative stressOzone

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.