COX5A over-expression protects cortical neurons from hypoxic ischemic injury in neonatal rats associated with TPI up-regulation [post]

2020 unpublished
Neonatal hypoxic-ischemic encephalopathy (HIE) is a destructive condition that constitutes a main cause of death in newborns. However, the underlying molecular mechanisms in brain damage are still not fully elucidated. Results: Here, we established hypoxic-ischemic (HI) injury and primary cortical neurons subjected to oxygen-glucose deprivation (OGD) to mimic HIE model in-vivo and in -vitro . Zea-longa scores, Triphenyte-trazoliumchloride (TTC) staining the Terminal Deoxynucleotidyl
more » ... eotidyl Transferased Utp Nick End Labeling (tunel) and immunofluorescent staining were used to detect the neurological injuries after HI. Then the expression of Cytochrome c oxidase subunit 5a (COX5A) was determined by immunohistochemistry, western blotting (WB) and quantitative real time Polymerase Chain Reaction (qRT-PCR) techniques. Moreover, HSV-mediated COX5A over-expression virus was administrated in -vitro to explore the role of COX5A in OGD neurons. Subsequently, the underlying mechanism was predicted by GeneMANIA and confirmed by WB and qRT-PCR. The results showed that HI induced a severe behavioral dysfunction, brain infarction, and cell apoptosis as well as obvious neuron loss in neonatal rats, in corresponding to the decrease on the expression of COX5A in both sides of the brain . What's more, COX5A overexpression significantly promoted the neuron survival, reduced the apoptosis rate, and markedly increased the neurites length after OGD. Moreover, Triosephosephate isomerase (TPI) was predicted as physical interactions with COX5A, and COX5A overexpression largely increased the expressional level of TPI. Conclusions: Together, these data suggest that COX5A plays an important role in promoting neurological recovery after HI, and this process is related to TPI up-
doi:10.21203/rs.2.20060/v1 fatcat:lxrr2fdmwndpnpvplmrsohaaxm