ArticleCell biochemistry and biophysics2026
Andrographolide Alleviates Inflammation in Chronic Obstructive Pulmonary Disease by Inhibiting Alveolar Macrophage Pyroptosis Through the JNK/NLRP3 Pathway.
Article in Cell biochemistry and biophysics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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.
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