ArticleMolecular medicine reports2015
Azithromycin attenuates cigarette smoke extract-induced oxidative stress injury in human alveolar epithelial cells.
Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 26 citations in OpenAlex.
- Benzo[a]pyrene aggravated ovalbumin‑induced epithelial tight junction disruption via ROS driven‑NLRP3/Caspase‑1 signaling pathway in asthmatic mice.International journal of molecular medicine · 2025Article
- Effects of azithromycin on lung oxidative injury and immune function in mice infected withCentral-European journal of immunology · 2025Article
- Erythromycin regulates peroxisome proliferator-activated receptor γ to ameliorate cigarette smoke-induced oxidative stress in macrophages.Journal of thoracic disease · 2024Article
- Azithromycin Mitigates Cisplatin-Induced Lung Oxidative Stress, Inflammation and Necroptosis by Upregulating SIRT1, PPARγ, and Nrf2/HO-1 Signaling.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Ninjinyoeito ameliorated cigarette smoke extract-induced apoptosis and inflammation through JNK signaling inhibition in human lung fibroblasts.BMC complementary medicine and therapies · 2022Article
- Cellular and Molecular Signatures of Oxidative Stress in Bronchial Epithelial Cell Models Injured by Cigarette Smoke Extract.International journal of molecular sciences · 2022Review
- Azithromycin ameliorates sulfur dioxide-induced airway epithelial damage and inflammatory responses.Respiratory research · 2020Article
- Using Phytochemicals to Investigate the Activation of Nicotine Detoxification via Upregulation of CYP2A6 in Animal Models Exposed Tobacco Smoke Condensate by Intratracheal Instillation.Evidence-based complementary and alternative medicine : eCAM · 2018Article
- The effect of electronic cigarette and tobacco smoke exposure on COPD bronchial epithelial cell inflammatory responses.International journal of chronic obstructive pulmonary disease · 2018Article
- Azithromycin attenuates myofibroblast differentiation and lung fibrosis development through proteasomal degradation of NOX4.Autophagy · 2017Article
- Effect of Phospholipid Transfer Protein on Cigarette Smoke Extract-Induced IL-8 Production in Human Pulmonary Epithelial Cells.Inflammation · 2016Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cigarette smoking has been verified to be one of the most important etiological factors causing the development of bronchogenic carcinoma and chronic obstructive pulmonary disease. Azithromycin (AZM) has been demonstrated to have antioxidant capacity. In the present study, whether AZM is able to attenuate cigarette smoke extract (CSE)‑induced A549 cell oxidative stress injury was investigated. Cells were incubated with CSE in the presence or absence of AZM. Cell viability was measured using a 3‑(4,5‑dimethylthiazol‑2‑yl)‑2,5‑diphenyltetrazolium bromide assay. The expression of vascular endothelial growth factor (VEGF) was analyzed using western blotting and ELISA. The expression of epithelial cell structural proteins, zona occludens (ZO)‑1 and occludin was determined using western blotting and immunofluorescence staining. Reactive oxygen species (ROS) production was examined by flow cytometry and fluorescence staining. The results demonstrated that the exposure of A549 cells to CSE decreased cell viability in a dose‑ and time‑dependent manner. AZM significantly attenuated the CSE‑induced decreases in the expression of VEGF and epithelial cell structural proteins, including ZO‑1 and occludin. CSE also stimulated ROS production in the A549 cell, while AZM significantly reversed the effects of CSE. In addition, the inhibition of ROS by N‑acetyl‑L‑cysteine had similar effects as AZM on the expression of VEGF and epithelial cell structural proteins and also enhanced cell proliferation. In conclusion, AZM attenuated CSE‑induced oxidative stress injury in A549 cells and may be a promising therapeutic agent for smoking‑associated pulmonary diseases.
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