Nicotine promotes chronic obstructive pulmonary disease via inducing pyroptosis activation in bronchial epithelial cells

Pyroptosis
DOI: 10.3892/mmr.2022.12608 Publication Date: 2022-02-09T17:16:58Z
ABSTRACT
Nicotine is one of the primary components in cigarettes, which responsible for addiction. Numerous studies have investigated effects nicotine on pulmonary disease. The health epithelial cells important development chronic obstructive disease (COPD). Accumulating evidence has suggested that cell death may initiate or contribute to progression a number lung diseases via airway remodeling. Pyroptosis unique form inflammatory mediated by activation caspase‑1 and NOD‑like receptor protein‑3 (NLRP3) inflammasome. present study aimed evaluate whether pyroptosis was involved COPD. normal human bronchial line 16HBE treated with 0.1 1 µM nicotine. Then proliferation ability detected CCK‑8. Cell flow cytometry analysis TUNEL assay. Subsequently, levels pro‑caspase 1, caspase IL‑1β, IL‑18, NLRP3, ASC cleaved GSDMD were examined western blotting. It revealed treatment significantly induced suppressed cells. Furthermore, exposure increased expression caspase‑1, apoptosis‑associated speck‑like protein gasdermin D Therefore, concluded cells, be associated
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