As hypothesized, co-treatment with IMP and either inhibitor substantially abrogated IMP’s ameliorative effects on LPS-induced pulmonary inflammation, histopathological damage, and oxidative stress in ALI mice, as evidenced by elevated inflammatory mediators (IL-1β, IL-6, and TNF-α) and total protein concentration in BALF (Fig. 8B, C), histopathological manifestations of alveolar collapse and thickened septal walls (Fig. 8D), and excessive ROS accumulation in lung tissue (Fig. 8E). The gene discussed is IL1B; the disease is acute respiratory distress syndrome.