Harmine Derivatives Alleviate LPS-Induced Acute Lung Injury via Targeting GSK3β

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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Publication Details

Journal
Inflammation
Published
2026-03-24
DOI
https://doi.org/10.1007/s10753-026-02487-6
Primary Topic
Synthesis and bioactivity of alkaloids
Type
article
Field-Weighted Citation Impact
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article

Harmine Derivatives Alleviate LPS-Induced Acute Lung Injury via Targeting GSK3β

Inflammation
Synthesis and bioactivity of alkaloids
article

Harmine Derivatives Alleviate LPS-Induced Acute Lung Injury via Targeting GSK3β

article en

Abstract

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.

Inflammation
Shenyang Pharmaceutical University (CN), Peking University (CN), General Hospital of Shenyang Military Region (CN), Peking University First Hospital (CN), Northeastern University (CN)
Openalex Percentile: Top 10%
Synthesis and bioactivity of alkaloids
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