炎症是许多急性和慢性疾病的重要病理过程，例如败血症、关节炎和癌症。许多因素可以导致机体出现炎症状态，其中细菌感染起着重要作用。细菌感染常导致败血症、急性肺损伤（ALI）或其更严重的急性呼吸窘迫综合征，这些是重症监护病房的主要致命疾病。已有报道称木犀草酮具有出色的抗炎活性，然而它是否能影响革兰阴性细菌引起的炎症仍不清楚。本研究中，以脂多糖（LPS）刺激小鼠腹腔巨噬细胞（MPM），使其释放促炎细胞因子，作为细胞模型。通过静脉注射和气管内注射LPS建立了小鼠脓毒症和ALI模型。本研究发现，木犀草酮通过IKK/NF-κB信号通路抑制了LPS诱导的巨噬细胞炎症反应。在体内，木犀草酮减轻了LPS诱导的小鼠败血症死亡。同时，木犀草酮治疗缓解了LPS诱导的肺损伤和炎症，通过抑制炎症细胞的浸润和炎症细胞因子的表达。综上所述，这些结果表明木犀草酮能够减轻革兰阴性细菌引起的炎症和疾病，可能是治疗炎症性疾病的潜在候选药物。© 2023. 作者及独家许可给Springer-Verlag GmbH Germany，隶属于Springer Nature。

Inflammation is an important pathological process of many acute and chronic diseases, such as sepsis, arthritis, and cancer. Many factors can lead to an inflammatory state of the body, among which bacterial infection plays an important role. Bacterial infection often leads to sepsis, acute lung injury (ALI), or its more serious form of acute respiratory distress syndrome, which are the main fatal diseases in intensive care units. Costunolide has been reported to possess excellent anti-inflammatory activity; however, whether it can affect inflammation induced by gram-negative bacterial is still unclear. Lipopolysaccharide (LPS) stimulated mouse peritoneal macrophages (MPMs) to release proinflammatory cytokines was used as the cell model. The mouse model of sepsis and ALI was built through injecting intravenously and intratracheally of LPS. In the present study, costunolide inhibited LPS-induced inflammatory response through IKK/NF-κB signaling pathway in macrophages. In vivo, costunolide attenuated LPS-induced septic death in mice. Meanwhile, costunolide treatment alleviated LPS-induced lung injury and inflammation via inhibiting the infiltration of inflammatory cells and the expression of inflammatory cytokines. Taken together, these results demonstrated that costunolide could attenuate gram-negative bacterial induced inflammation and diseases and might be a potential candidate for the treatment of inflammatory diseases.© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.