Scholarlink

<p>Traumatic brain injury (TBI) is a significant global health issue, characterized by high rates of morbidity and mortality, along with substantial economic strains on healthcare systems. This study explores the potential of Aminophylline (AMP), a medication traditionally used for cardiovascular conditions and bronchiectasis, to enhance TBI outcomes by protecting against neuronal damage. Our findings indicate that AMP treatment significantly reduces neuronal ferroptosis in the cortex, leading to less tissue damage and notable improvements in cognitive and motor functions in mice subjected to controlled cortical impact (CCI). Additionally, we found that TBI resulted in decreased expression of miR-128-3p, a reduction that was further strengthened by AMP treatment. Gain-of-function experiments showed that overexpressing miR-128-3p increases neuronal ferroptosis by targeting Slc7a11, indicating how AMP mitigates cognitive and motor impairments in CCI mice. This study highlights the potential of AMP in treating TBI through the miR-128-3p/Slc7a11 pathway, marking the first report of its protective effects against ferroptosis in TBI.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Aminophylline targets miR-128-3p/Slc7a11 axis to attenuate neuronal ferroptosis after traumatic brain injury

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年2月22日

查看全文
  • Li Manrui,
  • Yang Xu,
  • Jinyuan Liu,
  • Xiao Zhang,
  • Ruixuan Yuan,
  • Yuwen Sun,
  • Yihan Sun,
  • Qiuyun Yang,
  • Miao Liao,
  • Meili Lv,
  • Xin Hu,
  • Xiameng Chen,
  • Weibo Liang

摘要

Traumatic brain injury (TBI) is a significant global health issue, characterized by high rates of morbidity and mortality, along with substantial economic strains on healthcare systems. This study explores the potential of Aminophylline (AMP), a medication traditionally used for cardiovascular conditions and bronchiectasis, to enhance TBI outcomes by protecting against neuronal damage. Our findings indicate that AMP treatment significantly reduces neuronal ferroptosis in the cortex, leading to less tissue damage and notable improvements in cognitive and motor functions in mice subjected to controlled cortical impact (CCI). Additionally, we found that TBI resulted in decreased expression of miR-128-3p, a reduction that was further strengthened by AMP treatment. Gain-of-function experiments showed that overexpressing miR-128-3p increases neuronal ferroptosis by targeting Slc7a11, indicating how AMP mitigates cognitive and motor impairments in CCI mice. This study highlights the potential of AMP in treating TBI through the miR-128-3p/Slc7a11 pathway, marking the first report of its protective effects against ferroptosis in TBI.