Journal of ethnopharmacology · 2026
Cordyceps sinensis polysaccharide disrupts the macrophage pyroptosis-neutrophil extracellular traps axis to ameliorate acute lung injury.
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Xu Jingwen, Chen Sihan, Xie Shushu, Zhou Fangmei, Zhou Mingyuan, Ye Xiaoqing, Zhu Bingqi, Ding Zhishan, Chen Yuchi
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Cordyceps sinensis (Berk.) Sacc., a traditional Chinese medicine known for treating pulmonary diseases, contains vital bioactive polysaccharides. However, their specific therapeutic efficacy and underlying mechanisms in alleviating pulmonary inflammatory injury remain unclear.
AIM OF THE STUDY: This study aims to clarify the therapeutic effects of Cordyceps sinensis polysaccharide (CSP) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice and explored its underlying mechanism, focusing on the macrophage pyroptosis-neutrophil extracellular traps (NETs) signaling axis, to identify a potential ALI treatment.
MATERIALS AND METHODS: The mouse model of ALI was established via intratracheal instillation of LPS. CSP was administered via nebulization for intervention, with dexamethasone (DEX) serving as the positive control. Lung histopathology, immune cell infiltration, and inflammatory mediators were assessed by H&E, IHC, flow cytometry, Western blot, and qRT-PCR. Transcriptomic analysis was conducted to screen the core signaling pathways regulated by CSP. In vitro, a bone marrow-derived macrophage (BMDM) pyroptosis model and a pyroptotic extracellular vesicle (EV)-induced NETs formation system were utilized to verify the direct effects and molecular mechanism of CSP.
RESULTS: CSP significantly ameliorated ALI lung damage, restored lung barrier function, reduced pulmonary immune-inflammatory cell infiltration and systemic inflammation, and downregulated pro-inflammatory cytokines (IL-6, TNF-α). Transcriptomic analysis linked its effects to the NOD-like receptor and NETs formation pathways. Mechanistically, CSP inhibited macrophage NLRP3 inflammasome activation and pyroptosis. Crucially, CSP suppressed neutrophil NETs formation induced by pyroptotic macrophage-derived EVs, blocking the macrophage-neutrophil inflammatory cascade.
CONCLUSION: Targeting the macrophage pyroptosis-NETs signaling axis, CSP exerts multi-level inhibitory effects on excessive pulmonary inflammatory responses, providing significant therapeutic protection against ALI. These findings suggest CSP is a promising natural candidate drug for ALI treatment.
AIM OF THE STUDY: This study aims to clarify the therapeutic effects of Cordyceps sinensis polysaccharide (CSP) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice and explored its underlying mechanism, focusing on the macrophage pyroptosis-neutrophil extracellular traps (NETs) signaling axis, to identify a potential ALI treatment.
MATERIALS AND METHODS: The mouse model of ALI was established via intratracheal instillation of LPS. CSP was administered via nebulization for intervention, with dexamethasone (DEX) serving as the positive control. Lung histopathology, immune cell infiltration, and inflammatory mediators were assessed by H&E, IHC, flow cytometry, Western blot, and qRT-PCR. Transcriptomic analysis was conducted to screen the core signaling pathways regulated by CSP. In vitro, a bone marrow-derived macrophage (BMDM) pyroptosis model and a pyroptotic extracellular vesicle (EV)-induced NETs formation system were utilized to verify the direct effects and molecular mechanism of CSP.
RESULTS: CSP significantly ameliorated ALI lung damage, restored lung barrier function, reduced pulmonary immune-inflammatory cell infiltration and systemic inflammation, and downregulated pro-inflammatory cytokines (IL-6, TNF-α). Transcriptomic analysis linked its effects to the NOD-like receptor and NETs formation pathways. Mechanistically, CSP inhibited macrophage NLRP3 inflammasome activation and pyroptosis. Crucially, CSP suppressed neutrophil NETs formation induced by pyroptotic macrophage-derived EVs, blocking the macrophage-neutrophil inflammatory cascade.
CONCLUSION: Targeting the macrophage pyroptosis-NETs signaling axis, CSP exerts multi-level inhibitory effects on excessive pulmonary inflammatory responses, providing significant therapeutic protection against ALI. These findings suggest CSP is a promising natural candidate drug for ALI treatment.