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<p>Pyroptosis is involved in the progression of chronic obstructive pulmonary disease (COPD). Andrographolide (AG) possesses anti-inflammatory activity; however, its role in alveolar macrophage (AM) pyroptosis in COPD is still unclear. This study is to explore AG’s effects on AM pyroptosis and its underlying mechanism. A murine COPD model was generated by cigarette smoke (CS) exposure, and lung pathological changes were evaluated. A cigarette smoke extract (CSE)-induced MH-S cell model was established in vitro, with cells pretreated with AG or the c-jun N-terminal kinase (JNK) inhibitor SP600125. JNK activation and pyroptosis-related proteins were analyzed by Western blotting, while proinflammatory cytokines in bronchoalveolar lavage fluid and MH-S cell supernatants were measured by ELISA. CS exposure impaired lung function, induced alveolar enlargement and inflammatory cell infiltration, all of which were alleviated by AG treatment. JNK phosphorylation, pyroptosis-associated protein expression, and cytokine production were increased in COPD murine models and CSE-stimulated MH-S cells. Importantly, these effects induced by CSE in MH-S cells were suppressed by SP600125. Notably, AG exerted similar inhibitory effects. In conclusion, AG attenuates CS-induced inflammation in COPD via suppressing JNK/NLRP3-dependent AM pyroptosis. This finding identifies a novel mechanism of AG action and verifies JNK as its core regulatory molecule.</p>

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Andrographolide Alleviates Inflammation in Chronic Obstructive Pulmonary Disease by Inhibiting Alveolar Macrophage Pyroptosis Through the JNK/NLRP3 Pathway

  • 期刊论文

  • 发表日期：

    2026年3月11日

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  • Tingting Zhang,
  • Xiaofeng Li,
  • Zhe Wang,
  • Xin Li,
  • Ping Huang,
  • Xiaoli Zeng,
  • Xiaoju Liu

摘要

Pyroptosis is involved in the progression of chronic obstructive pulmonary disease (COPD). Andrographolide (AG) possesses anti-inflammatory activity; however, its role in alveolar macrophage (AM) pyroptosis in COPD is still unclear. This study is to explore AG’s effects on AM pyroptosis and its underlying mechanism. A murine COPD model was generated by cigarette smoke (CS) exposure, and lung pathological changes were evaluated. A cigarette smoke extract (CSE)-induced MH-S cell model was established in vitro, with cells pretreated with AG or the c-jun N-terminal kinase (JNK) inhibitor SP600125. JNK activation and pyroptosis-related proteins were analyzed by Western blotting, while proinflammatory cytokines in bronchoalveolar lavage fluid and MH-S cell supernatants were measured by ELISA. CS exposure impaired lung function, induced alveolar enlargement and inflammatory cell infiltration, all of which were alleviated by AG treatment. JNK phosphorylation, pyroptosis-associated protein expression, and cytokine production were increased in COPD murine models and CSE-stimulated MH-S cells. Importantly, these effects induced by CSE in MH-S cells were suppressed by SP600125. Notably, AG exerted similar inhibitory effects. In conclusion, AG attenuates CS-induced inflammation in COPD via suppressing JNK/NLRP3-dependent AM pyroptosis. This finding identifies a novel mechanism of AG action and verifies JNK as its core regulatory molecule.