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<p>Ferroptosis is a death mode centered on iron metabolism and lipid peroxidation pathways. Recent studies have shown that inhibiting ferroptosis can alleviate intestinal ischemia/reperfusion (II/R) injury. Hydrogen (H<sub>2</sub>) can mitigate II/R injury by anti-oxidative stress, while Silicon (Si)-based agent can generate a large amount of H<sub>2</sub> in the alkaline environment of the intestine during II/R. However, it is unclear whether Si-based agent can alleviate II/R injury. By establishing a mouse model of II/R injury, we examined the histopathological changes, apoptosis, inflammatory factors, oxidative stress, and ferroptosis levels in the small intestine. We found that the AMPK-Sirt1 pathway is activated in the small intestine of mice after II/R, and Si-based agent can further activate this pathway, alleviating intestinal injury, inhibiting apoptosis, reversing inflammation and oxidative stress, and suppressing ferroptosis in mice after II/R. Furthermore, by administering AMPK agonists and inhibitors, as well as ferroptosis inhibitors for further exploration, we discovered that the hydrogen generated by Si-based agent may inhibit ferroptosis and alleviate II/R injury through the AMPK-Sirt1 signaling pathway. This study provides theoretical and experimental evidence for elucidating the pathogenesis of intestinal ischemia/reperfusion injury and for the clinical application of Si-based agent.</p>

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Silicon-based agent alleviating intestinal ischemia/reperfusion injury in mice by inhibiting ferroptosis via activating AMPK-Sirt1 signaling pathway

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年5月19日

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  • Xiao Liu,
  • Binglong Wang,
  • Xujiao Wang,
  • Qin Ye,
  • Jianfei Wu,
  • Guo Mu

摘要

Ferroptosis is a death mode centered on iron metabolism and lipid peroxidation pathways. Recent studies have shown that inhibiting ferroptosis can alleviate intestinal ischemia/reperfusion (II/R) injury. Hydrogen (H2) can mitigate II/R injury by anti-oxidative stress, while Silicon (Si)-based agent can generate a large amount of H2 in the alkaline environment of the intestine during II/R. However, it is unclear whether Si-based agent can alleviate II/R injury. By establishing a mouse model of II/R injury, we examined the histopathological changes, apoptosis, inflammatory factors, oxidative stress, and ferroptosis levels in the small intestine. We found that the AMPK-Sirt1 pathway is activated in the small intestine of mice after II/R, and Si-based agent can further activate this pathway, alleviating intestinal injury, inhibiting apoptosis, reversing inflammation and oxidative stress, and suppressing ferroptosis in mice after II/R. Furthermore, by administering AMPK agonists and inhibitors, as well as ferroptosis inhibitors for further exploration, we discovered that the hydrogen generated by Si-based agent may inhibit ferroptosis and alleviate II/R injury through the AMPK-Sirt1 signaling pathway. This study provides theoretical and experimental evidence for elucidating the pathogenesis of intestinal ischemia/reperfusion injury and for the clinical application of Si-based agent.