支气管肺泡灌洗
药理学
脂多糖
肺
一氧化氮
炎症
医学
去氢骆驼蓬碱
细胞因子
一氧化氮合酶
化学
免疫学
细胞毒性
渗透(HVAC)
细胞内
NF-κB
促炎细胞因子
下调和上调
作者
Xinhui Ye,Junjie Lin,Tianqi Zhang,Huanhua Chen,Hui Huang,Lingyu Cui,Jiacheng Zhuang,Mingzuo Zhang,Wenwu Liu,Wenjie Liu,Limeng Wu,Bolin Du,Ying Chen,Qiong Wu,Zihua Xu,Xi Zeng,Qingchun Zhao
出处
期刊:Inflammation
[Springer Science+Business Media]
日期:2026-03-24
卷期号:49 (1)
标识
DOI:10.1007/s10753-026-02487-6
摘要
Acute lung injury (ALI) is a life-threatening inflammatory disorder with limited therapeutic options. This study evaluated the anti-inflammatory activity of ZLWH-38, a novel harmine derivative, in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages and a murine ALI model. ZLWH-38 showed low cytotoxicity and effectively inhibited the production of nitric oxide and pro-inflammatory cytokines. In macrophages, it dose-dependently reduced the expression of TNF-α, IL-6, IL-1β and iNOS, and intracellular ROS levels. Mechanistic investigations indicated that ZLWH-38 interacted with glycogen synthase kinase-3β (GSK3β) and suppressed downstream NF-κB signaling. In female C57BL/6 mice subjected to LPS-induced lung injury, prophylactic administration of ZLWH-38 markedly attenuated histopathological damage, lowered the lung wet/dry weight ratio, and decreased neutrophil infiltration and cytokine levels in bronchoalveolar lavage fluid and lung tissue. These findings suggest that ZLWH-38 ameliorates ALI by blocking GSK3β and thereby repressing downstream NF-κB signaling to curtail inflammation, offering a novel rationale and mechanistic foundation for ALI therapeutics.
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