COX5A Relieves Traumatic Brain Injury-Induced Neurological Damage in Mice by Correcting Mitochondrial Homeostasis Imbalance

Guangcai LIU; Hongchen HUANG; Honglan CHEN; Shui JIANG; Yanbin XIYANG; Xu YANG

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Guangcai LIU, Hongchen HUANG, Honglan CHEN, Shui JIANG, Yanbin XIYANG, Xu YANG. COX5A Relieves Traumatic Brain Injury-Induced Neurological Damage in Mice by Correcting Mitochondrial Homeostasis Imbalance[J]. Journal of Kunming Medical University.

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COX5A Relieves Traumatic Brain Injury-Induced Neurological Damage in Mice by Correcting Mitochondrial Homeostasis Imbalance

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Received Date: 2025-11-16

Abstract

Abstract

Objective To investigate the neuroprotective effect of cytochrome c oxidase subunit 5A （COX5A） overexpression in mice with traumatic brain injury （TBI） and its association with mitochondrial function. Methods C57BL/6J wild-type （WT） mice aged 4–6 weeks and age-matched COX5A-overexpressing （COX5A-UP） transgenic mice were randomly divided into WT+sham operation group, WT+TBI group, COX5A-UP+sham operation group, and COX5A-UP+TBI group （n = 12 per group, male∶female = 1∶1）. The TBI model was established using the controlled cortical impact method. At 14 days after surgery, neurological and behavioral performance, brain water content, oxygen consumption rate of hippocampal synaptosomal mitochondrial , ATP levels, reactive oxygen species, malondialdehyde, mitochondrial membrane potential and mitochondrial ultrastructure were examined. Results Compared with the WT+sham group, WT+TBI group showed impaired neurological and behavioral performance, increased brain water content, reduced mitochondrial energy metabolism, enhanced oxidative stress and mitochondrial morphological damage （P < 0.05）. Compared with the WT+TBI group, the COX5A-UP+TBI group showed improvements in these neurological, behavioral, edema-related and mitochondrial abnormalities （P < 0.05）. Conclusion COX5A overexpression alleviates TBI-induced neurological impairment, and this effect may be associated with amelioration of synaptosomal mitochondrial dysfunction and preservation of mitochondrial structural homeostasis.
- COX5A,
- Traumatic Brain Injury,
- Mitochondrial Dyshomeostasis,
- Neuroprotection,
- Mouse Model,
- Behavior

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References(21)

References

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