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<p>Sepsis-induced acute lung injury is a life-threatening complication with limited therapeutic options. Although the gut-lung axis is crucial in sepsis pathogenesis, effective interventions targeting this pathway remain scarce. Here, we developed multi-enzymatic platinum-doped emodin carbon dots (Pt-ECDs) via a hydrothermal method. Pt-ECDs exhibited superior catalase, superoxide dismutase, glutathione peroxidase and peroxidase-like activities, enabling potent reactive oxygen species (ROS) scavenging. In a murine sepsis model, oral Pt-ECDs significantly improved survival, reduced systemic inflammation, and ameliorated lung injury. Transcriptomic analysis revealed that Pt-ECDs suppressed oxidative stress and macrophage pyroptosis in lung tissues. Mechanistically, integrated metabolomic and microbiome analyses demonstrated that Pt-ECDs modulated the gut microbiota, specifically inhibiting g_Bacteroides-derived palmitic acid (PA) production. We further confirmed that PA exacerbates macrophage pyroptosis and pro-inflammatory polarization by directly binding to NOX2 and NLRP3. Crucially, fecal microbiota transplantation from Pt-ECDs-treated mice attenuated septic lung injury, whereas microbiota depletion abolished the therapeutic benefits. Collectively, our findings identify Pt-ECDs as a promising nanotherapeutic that alleviates septic lung injury by targeting the gut microbiota-palmitic acid-pyroptosis axis.</p> Graphical abstract <p></p>

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Platinum-doped emodin carbon dots mitigate sepsis-induced lung injury by targeting the gut-lung axis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年12月26日

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  • Honghao Song,
  • Yuqing Ma,
  • Lei Peng,
  • Fangyuan Gao,
  • Xiaoyi Fan,
  • Mei Yang,
  • Tong Hua,
  • Yutong Yang,
  • Rongrong Fan,
  • Zhenjie Li,
  • Hongbin Yuan

摘要

Sepsis-induced acute lung injury is a life-threatening complication with limited therapeutic options. Although the gut-lung axis is crucial in sepsis pathogenesis, effective interventions targeting this pathway remain scarce. Here, we developed multi-enzymatic platinum-doped emodin carbon dots (Pt-ECDs) via a hydrothermal method. Pt-ECDs exhibited superior catalase, superoxide dismutase, glutathione peroxidase and peroxidase-like activities, enabling potent reactive oxygen species (ROS) scavenging. In a murine sepsis model, oral Pt-ECDs significantly improved survival, reduced systemic inflammation, and ameliorated lung injury. Transcriptomic analysis revealed that Pt-ECDs suppressed oxidative stress and macrophage pyroptosis in lung tissues. Mechanistically, integrated metabolomic and microbiome analyses demonstrated that Pt-ECDs modulated the gut microbiota, specifically inhibiting g_Bacteroides-derived palmitic acid (PA) production. We further confirmed that PA exacerbates macrophage pyroptosis and pro-inflammatory polarization by directly binding to NOX2 and NLRP3. Crucially, fecal microbiota transplantation from Pt-ECDs-treated mice attenuated septic lung injury, whereas microbiota depletion abolished the therapeutic benefits. Collectively, our findings identify Pt-ECDs as a promising nanotherapeutic that alleviates septic lung injury by targeting the gut microbiota-palmitic acid-pyroptosis axis.

Graphical abstract