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<p>As a disease of high mortality rate, acute lung injury (ALI) has been getting increased attention. Heme oxygenase-1 (HO-1), which plays an essential role in alleviating the pathological symptoms of ALI. There have few studies noted that the improvement effect of HO-1 on ALI may associated to NOD-like receptor protein 3 (NLRP3) inflammasome. However, the roles of HO-1 in the process of NLRP3 inflammasome activation is remains unknown. This study investigated the mechanism that HO-1 blocking NLRP3 inflammasome in ALI. The sepsis model induced by LPS was used in C57BL6 mice, LPS triggered obviously pulmonary damage and edema formation, increased the expression of NLRP3 inflammasome component proteins and IL-1β, but those negative effects were reversed by the pretreatment of hemin. NOD-like receptor signaling pathway was down-regulated after hemin treatment through RNA-Seq.&#xa0;Meanwhile, hemin pretreatment exerted significantly inhibit effect on the activation of NLRP3 inflammasome, and the component proteins of NLRP3 inflammasome were not influenced in immortalization of bone marrow-derived macrophages (iBMDMs). Moreover, the immunoprecipitation and immunofluorescence experiments were indicated that HO-1 could bind to NLRP3, silencing HO-1 prevented the block effect of hemin on NLRP3 inflammasome activation. Our study suggested that hemin-inhibited NLRP3 inflammasome activation involved HO-1 bind to NLRP3 and alleviated ALI mice induced by LPS.</p>

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Induction of heme oxygenase-1 by hemin alleviates acute lung injury through inhibition of NLRP3 inflammasome assembly

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月14日

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  • Xinyue Gao,
  • Long You,
  • Luyao Qi,
  • Lei Jin,
  • Jianmei Zhang,
  • Yanan Liu,
  • Zhiqiang Niu

摘要

As a disease of high mortality rate, acute lung injury (ALI) has been getting increased attention. Heme oxygenase-1 (HO-1), which plays an essential role in alleviating the pathological symptoms of ALI. There have few studies noted that the improvement effect of HO-1 on ALI may associated to NOD-like receptor protein 3 (NLRP3) inflammasome. However, the roles of HO-1 in the process of NLRP3 inflammasome activation is remains unknown. This study investigated the mechanism that HO-1 blocking NLRP3 inflammasome in ALI. The sepsis model induced by LPS was used in C57BL6 mice, LPS triggered obviously pulmonary damage and edema formation, increased the expression of NLRP3 inflammasome component proteins and IL-1β, but those negative effects were reversed by the pretreatment of hemin. NOD-like receptor signaling pathway was down-regulated after hemin treatment through RNA-Seq. Meanwhile, hemin pretreatment exerted significantly inhibit effect on the activation of NLRP3 inflammasome, and the component proteins of NLRP3 inflammasome were not influenced in immortalization of bone marrow-derived macrophages (iBMDMs). Moreover, the immunoprecipitation and immunofluorescence experiments were indicated that HO-1 could bind to NLRP3, silencing HO-1 prevented the block effect of hemin on NLRP3 inflammasome activation. Our study suggested that hemin-inhibited NLRP3 inflammasome activation involved HO-1 bind to NLRP3 and alleviated ALI mice induced by LPS.