These findings were consistent with several previous studies in vitro and in vivo that fisetin inhibited the production of pro-inflammatory mediators through suppression of NF-κB, JNK, and other immune-related signaling pathways in LPS-treated macrophages (28, 30, 31), and exerted anti-inflammatory activity in LPS-induced colitis (32), acute lung injury (33), central nervous system-insult (34), and acute otitis (35). The gene discussed is NFKB1; the disease is acute lung injury.