EA-BN downregulated thioredoxin-interacting protein and NLRP3 inflammasome activation, thereby suppressing caspase-1 and IL-1β expression, whereas also attenuating apoptosis by modulating the Bax/Bcl-2/caspase-3 pathway.<h4>Discussion</h4>Collectively, these findings suggest that EA-BN possesses antioxidant, anti-inflammatory, and anti-apoptotic properties, supporting its potential as a preventive agent against COPD. The gene discussed is CASP1; the disease is chronic obstructive pulmonary disease.