ALI is a severe clinical syndrome with limited treatment options beyond corticosteroids, which cause significant adverse effects. This study demonstrates that the herbal combination EAC significantly attenuates LPS-induced ALI through dual pathway inhibition. EAC suppresses TLR4/NF-κB and NLRP3 inflammasome signaling, thereby inhibiting MyD88-mediated NF-κB activation, NLRP3 inflammasome assembly, caspase-1 activation, and GSDMD-|mediated pyroptosis. Consequently, EAC reduces proinflammatory cytokine production (IL-1β, IL-18) and restores the balance between inflammatory and anti-inflammatory responses, offering a promising therapeutic alternative to conventional corticosteroids for ALI treatment.