MPO-Mediated oxidative stress regulates lung tissue damage in T-COPD through activation of the NLRP3 inflammasome.

PURPOSE: -induced chronic obstructive pulmonary disease (T-COPD) model. METHODS: with or without MPO treatment, followed by assessments of cell viability, apoptosis, ROS levels, and NLRP3 pathway activity. RESULTS: , MPO treatment exacerbated NLRP3 activation in murine lung epithelial MLE-12 cells, while MPO inhibition (with MPO-IN-5) or NLRP3 knockdown mitigated these effects, enhancing cell proliferation and reducing apoptosis. CONCLUSION: Our results suggest that MPO plays a critical role in regulating the NLRP3 signaling pathway, contributing to lung injury in the T-COPD model. Inhibition of MPO with MPO-IN-5 effectively alleviates inflammation, reduces oxidative stress, and suppresses NLRP3 pathway activation, highlighting its potential as a therapeutic target for T-COPD.