Hepcidin attenuates the iron-mediated secondary neuronal injury after intracerebral hemorrhage in rats

Iron plays a key role in secondary neuronal injury after intracerebral hemorrhage (ICH), and hepcidin is able to reduce brain iron in iron-overloaded rats by down-regulating iron transport proteins including ferroportin 1 and transferrin receptor 1. These led us to hypothesize that hepcidin might reduce iron-mediated neurotoxicity by inhibiting iron accumulation in ICH brain. Here, we examined effects of Ad-hepcidin (hepcidin expression adenovirus) on the non-heme iron contents, expression of hepcidin, ferritin and iron transport proteins, neuronal cell survival, water contents in the brain and/or cerebrospinal fluid (CSF), and ICH-induced apoptosis, neurological deficit by RT-PCR, Western blot analysis, NeuN Immunofluorescence, TUNEL, Fluoro-Jade B staining, behavioral performance and Morris water-maze tests in 510 rats.

Source: Translational Research - September 10, 2020 Category: Research Authors: Guang Yang, Christopher Qian, Chao Zhang, Yong Bao, Meng-Yue Liu, Fei Jiang, Wei Li, Yong Liu, Ya Ke, Zhong-Ming Qian Tags: Original article Source Type: research