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ABSTRACT: Aim
We aimed to investigate the regulatory role of Netrin-1 (NTN1) in ferroptosis after traumatic brain injury (TBI) in mice.Methods
We assessed the expression pattern of NTN1 by RT-PCR, western blot, and immunofluorescence after establishing the TBI model in mice. After treatment with NTN1 shRNA or recombinant NTN1, we determined the biochemical and morphological changes associated with ferroptosis and netrin-1-related pathways. We used Nissl staining to assess lesion volume and Morris water maze and beam-walking test to evaluate ethological manifestation.Results
The mRNA and protein levels of NTN1 were upregulated after TBI. The application of NTN1 shRNA increased the number of FJB positive cells, malondialdehyde (MDA), and reactive oxygen species (ROSs) levels. H
SUBMITTER: Zhang Y
PROVIDER: S-EPMC9804081 | biostudies-literature | 2023 Jan
REPOSITORIES: biostudies-literature