BMSCs alleviate inflammation and inhibit apoptosis in radiation pneumonitis treatment by modulating the NF-κB/NLRP3 signaling pathway

Radiation pneumonitis (RP) is a severe consequence of thoracic radiation, and its pathophysiology is tightly linked to NLRP3 inflammasome-mediated hyperinflammatory reactions. The nuclear factor κB (NF-κB) signaling system, which regulates NLRP3, could be a potential therapeutic target. This study explores how bone marrow-derived mesenchymal stem cells (BMSCs) can treat RP via modifying the NF-κB/NLRP3 signaling pathway. BMSCs treatment significantly reduced inflammatory infiltration in rat lung tissue and decreased inflammatory cytokine release. Mechanistically, by inhibiting the NF-κB/NLRP3 signaling axis, BMSCs consequently reduce the secretion of key pro-inflammatory mediators, including IL-1β, IL-18, and TNF-α. Additionally, BMSCs suppressed apoptosis by downregulating inflammasome formation, achieving therapeutic effects against RP. BMSCs block NF-κB/NLRP3 signaling, reducing inflammasome production. They treat RP by inhibiting inflammasomes and suppressing apoptosis. This strategy is a novel therapy option for RP management and clinical prevention.