Acute lung injury (ALI) is characterized by excessive inflammatory responses in lung tissue and the antiinflammatory agent is proposed to be a therapeutic drugs for ALI. Bisabolol has been demonstrated to have antiinflammatory activity through inhibiting the activation of NF-kB (nuclear factor kappa B). However, it is still unknown whether the bisabolol possesses the protective effect on ALI. In this study, we assessed the effect of bisabolol on the lung inflammation caused by sepsis in mice. We found that bisabolol pretreatment could markedly improve the histology of the lung and suppress the lung inflammation, such as the production of inflammatory cytokines in bronchoalveolar lavage fluid (BALF). Meanwhile, the lung wet/dry ratio, myeloperoxidase (MPO) activity, total inflammatory cells and production of nitric oxide (NO) in lung tissue, induced by sepsis, were reduced by bisabolol treatment. Additionally, bisabolol treatment also inhibited the degradation of IkB-alpha (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha), subsequently blocked the activation of NF-kB pathway caused by sepsis in vivo. Bisabolol could attenuate sepsis-induced lung injury in mice through inhibiting NF-kB signaling in macrophages, suggesting bisabolol might be a potential therapeutic candidate for the treatment of sepsis-induced lung injury.