{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,1]],"date-time":"2026-06-01T09:07:17Z","timestamp":1780304837320,"version":"3.54.0"},"reference-count":39,"publisher":"Brieflands","issue":"1","license":[{"start":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T00:00:00Z","timestamp":1773446400000},"content-version":"am","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["brieflands.com"],"crossmark-restriction":false},"short-container-title":["Iran J Pharm Res"],"abstract":"<jats:p>Background: Mycoplasma pneumoniae pneumonia (MPP) is a pulmonary inflammatory disease caused by Mycoplasma pneumoniae (Mp) infection that primarily involves the bronchi, alveoli, and pulmonary interstitium. It is the most common cause of community-acquired pneumonia in children. Andrographolide (AG) is a natural diterpenoid lactone with anti-inflammatory and immunomodulatory activities; however, its specific role and mechanism in MPP remain unclear. Objectives: This study aimed to investigate the mechanism by which AG inhibits pyroptosis in alveolar epithelial cells via the HMGB1\/TLR4\/NF-\u03baB signaling pathway in the treatment of MPP in children. Methods: Mp-stimulated MLE-12 cells were treated with AG at 10, 20, or 50 \u03bcM. Cell viability and injury were assessed using CCK-8 and LDH assays, respectively. Protein expression levels of NLRP3, HMGB1, TLR4, and p-NF-\u03baB p65 were determined by Western blotting, and cytokine levels (IL-6 and TNF-\u03b1) were measured by ELISA. In an Mp-infected mouse model, mice received AG at 25 or 50 mg\/kg. Body weight, lung index, lung histopathology, pathway-related protein expression, and cytokine levels (IL-1\u03b2 and TNF-\u03b1) in bronchoalveolar lavage fluid (BALF) were evaluated. Results: Mp significantly induced cytotoxicity, pyroptosis, and inflammation in vitro and in vivo (all P &lt; 0.001). Andrographolide treatment dose-dependently reduced LDH release, suppressed HMGB1\/TLR4\/NF-\u03baB\/NLRP3 activation, and decreased proinflammatory cytokine levels (P &lt; 0.05). In mice, AG improved survival-related metrics, ameliorated lung pathology, and inhibited pathway activity and cytokine secretion. Conclusions: Andrographolide mitigates MPP via the HMGB1\/TLR4\/NF-\u03baB signaling pathway by inhibiting pulmonary epithelial cell pyroptosis and inflammation. These findings indicate its potential as a therapeutic agent.<\/jats:p>","DOI":"10.5812\/ijpr-169826","type":"journal-article","created":{"date-parts":[[2026,6,1]],"date-time":"2026-06-01T08:33:04Z","timestamp":1780302784000},"update-policy":"https:\/\/doi.org\/10.5812\/crossmark_update_policy","source":"Crossref","is-referenced-by-count":0,"title":["Andrographolide Alleviates &lt;i&gt;Mycoplasma pneumoniae&lt;\/i&gt; Pneumonia in Children by Inhibiting Alveolar Epithelial Cell Pyroptosis Through the HMGB1\/TLR4\/NF-\u03baB 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