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<p>This study aimed to explore the protective mechanism of bilirubin (Bil) against cigarette smoke extract (CSE)-induced inflammation and lung tissue damage and offer a new target and theoretical foundation for preventing and treating CSE-induced respiratory diseases. Wistar rats in the CSE group were exposed to CSE via nasal drip for 8 weeks; CSE + Bil group rats received bilirubin (20&#xa0;mg/kg) by gavage 30&#xa0;min before each daily CSE instillation for 8 weeks; and control group rats received the intervention of an equal volume of the vehicle following the same schedule. After eight weeks, lung function, pathological change, oxidative stress, mitochondrial function, pyroptosis-related proteins, and inflammatory cytokines were assessed. CSE damaged lung function and tissue by inducing oxidative stress damage and mitochondrial dysfunction as well as triggering macrophage pyroptosis-related inflammation, manifesting as decreased adenosine triphosphate (ATP) and SOD levels, increased MDA, and elevated macrophage pyroptosis-related proteins expressions and inflammatory cytokine levels, whereas Bil reduced CSE-induced mitochondrial dysfunction, suppressed oxidative stress, alleviated macrophage pyroptosis and inflammation, improved lung tissue pathological injury, and enhanced lung function. Bil treatment improved pathological lung damage and enhanced lung function by reducing mitochondrial dysfunction, maintaining the redox balance, and alleviating CSE-induced macrophage pyroptosis and inflammation in the lung tissue.</p>

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Bilirubin alleviates cigarette smoke extract-induced lung tissue inflammation and damage by suppressing macrophage pyroptosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年8月1日

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  • Guoquan Fan,
  • Meiqi Guan,
  • Chunli Xu,
  • Yuan Tian,
  • Jianing Xie,
  • Jingjing Wei

摘要

This study aimed to explore the protective mechanism of bilirubin (Bil) against cigarette smoke extract (CSE)-induced inflammation and lung tissue damage and offer a new target and theoretical foundation for preventing and treating CSE-induced respiratory diseases. Wistar rats in the CSE group were exposed to CSE via nasal drip for 8 weeks; CSE + Bil group rats received bilirubin (20 mg/kg) by gavage 30 min before each daily CSE instillation for 8 weeks; and control group rats received the intervention of an equal volume of the vehicle following the same schedule. After eight weeks, lung function, pathological change, oxidative stress, mitochondrial function, pyroptosis-related proteins, and inflammatory cytokines were assessed. CSE damaged lung function and tissue by inducing oxidative stress damage and mitochondrial dysfunction as well as triggering macrophage pyroptosis-related inflammation, manifesting as decreased adenosine triphosphate (ATP) and SOD levels, increased MDA, and elevated macrophage pyroptosis-related proteins expressions and inflammatory cytokine levels, whereas Bil reduced CSE-induced mitochondrial dysfunction, suppressed oxidative stress, alleviated macrophage pyroptosis and inflammation, improved lung tissue pathological injury, and enhanced lung function. Bil treatment improved pathological lung damage and enhanced lung function by reducing mitochondrial dysfunction, maintaining the redox balance, and alleviating CSE-induced macrophage pyroptosis and inflammation in the lung tissue.