Iron has a key role in the activation of the autophagic pathway in rats with intracerebral hemorrhage (ICH), and hepcidin has the ability to reduce brain iron in ICH-rats. We therefore hypothesized that hepcidin might be able to inhibit autophagy by reducing iron in an ICH brain. Here, we investigated the effects of Ad-hepcidin and/or hepcidin peptide on autophagic activities in ICH models in vitro and in vivo. We demonstrated that ad-hepcidin and hepcidin peptide both inhibited hemin-induced increase in LC3-II/LC3-I conversion ratio and reversed the reduction in p62 content in cortical neurons in vitro. We also showed that ad-hepcidin inhibited ICH-induced increase in LC3-II/LC3-I conversion ratio and reversed ICH-induced reduction in p62 content in the brain cortex of rats in vivo. Based on these findings plus previous data on the effects of ad-hepcidin and/or hepcidin peptide on iron contents in ICH models, we suggested that hepcidin-induced inhibition of autophagy might be mediated via reducing iron in hemin-treated neurons in vitro and ICH-rat brain in vivo.

铁在脑出血 (ICH) 大鼠的自噬通路激活中起关键作用，铁调素具有降低 ICH 大鼠脑铁的能力。因此，我们假设铁调素可能能够通过减少 ICH 大脑中的铁来抑制自噬。在这里，我们在体外和体内研究了 Ad-hepcidin 和/或 hepcidin 肽对 ICH 模型中自噬活性的影响。我们证明，ad-hepcidin 和 hepcidin 肽都抑制了血红素诱导的 LC3-II/LC3-I 转化率的增加，并在体外逆转了皮层神经元中 p62 含量的减少。我们还表明，ad-hepcidin 抑制了 ICH 诱导的 LC3-II/LC3-I 转化率的增加，并在体内逆转了 ICH 诱导的大鼠大脑皮层 p62 含量的减少。