Background: Neonatal hypoxic-ischemic encephalopathy (HIE) represents as a major cause of neonatal morbidity and mortality. However, the underlying molecular mechanisms in brain damage are still not fully elucidated. This study was conducted to determine the specific potential molecular mechanism in the hypoxic-ischemic induced cerebral injury.
Methods: Here, hypoxic-ischemic (HI) animal models were established and primary cortical neurons were subjected to oxygen-glucose deprivation (OGD) to mimic HIE model in-vivo and in-vitro. The HI-induced neurological injury was evaluated by Zea-longa scores, Triphenyte-trazoliumchloride (TTC) staining the Terminal Deoxynucleotidyl Transferased Utp Nick End Labeling (TUNEL) and immunofluorescent staining. 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 transducted into OGD neurons to explore the role of COX5A in-vitro, and the underlying mechanism was predicted by GeneMANIA, then verified by WB and qRT-PCR.
Results: HI induced a severe neurological 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 over-expression significantly promoted the neuronal 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 over-expression largely increased the expressional level of TPI.
Conclusions: The present findings suggest that COX5A plays an important role in promoting neurological recovery after HI, and this process is related to TPI up-regulation.
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Posted 15 Apr, 2020
On 11 Apr, 2020
On 18 Mar, 2020
Received 14 Mar, 2020
Received 12 Mar, 2020
Invitations sent on 08 Mar, 2020
On 08 Mar, 2020
On 08 Mar, 2020
On 02 Mar, 2020
On 01 Mar, 2020
On 01 Mar, 2020
On 17 Jan, 2020
Received 14 Jan, 2020
Received 10 Jan, 2020
On 04 Jan, 2020
Invitations sent on 03 Jan, 2020
On 03 Jan, 2020
On 31 Dec, 2019
On 30 Dec, 2019
On 30 Dec, 2019
Posted 15 Apr, 2020
On 11 Apr, 2020
On 18 Mar, 2020
Received 14 Mar, 2020
Received 12 Mar, 2020
Invitations sent on 08 Mar, 2020
On 08 Mar, 2020
On 08 Mar, 2020
On 02 Mar, 2020
On 01 Mar, 2020
On 01 Mar, 2020
On 17 Jan, 2020
Received 14 Jan, 2020
Received 10 Jan, 2020
On 04 Jan, 2020
Invitations sent on 03 Jan, 2020
On 03 Jan, 2020
On 31 Dec, 2019
On 30 Dec, 2019
On 30 Dec, 2019
Background: Neonatal hypoxic-ischemic encephalopathy (HIE) represents as a major cause of neonatal morbidity and mortality. However, the underlying molecular mechanisms in brain damage are still not fully elucidated. This study was conducted to determine the specific potential molecular mechanism in the hypoxic-ischemic induced cerebral injury.
Methods: Here, hypoxic-ischemic (HI) animal models were established and primary cortical neurons were subjected to oxygen-glucose deprivation (OGD) to mimic HIE model in-vivo and in-vitro. The HI-induced neurological injury was evaluated by Zea-longa scores, Triphenyte-trazoliumchloride (TTC) staining the Terminal Deoxynucleotidyl Transferased Utp Nick End Labeling (TUNEL) and immunofluorescent staining. 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 transducted into OGD neurons to explore the role of COX5A in-vitro, and the underlying mechanism was predicted by GeneMANIA, then verified by WB and qRT-PCR.
Results: HI induced a severe neurological 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 over-expression significantly promoted the neuronal 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 over-expression largely increased the expressional level of TPI.
Conclusions: The present findings suggest that COX5A plays an important role in promoting neurological recovery after HI, and this process is related to TPI up-regulation.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
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