ArticleJournal of biosciences2013
Effect of normabaric hyperoxia treatment on neuronal damage following fluid percussion injury in the striatum of mice: a morphological approach.
Article in Journal of biosciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Preclinical progenitor cell therapy in traumatic brain injury: a meta-analysis.The Journal of surgical research · 2017Pooled it
- Normobaric oxygen worsens outcome after a moderate traumatic brain injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015Article
- Normobaric hyperoxia is associated with increased cerebral excitotoxicity after severe traumatic brain injury.Neurocritical care · 2015Article
- Normabaric Hyperoxia Treatment Improved Locomotor Activity of C57BL/6J Mice through Enhancing Dopamine Genes Following Fluid-Percussion Injury in Striatum.International journal of biomedical science : IJBS · 2013Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) causes significant mortality in most developing countries worldwide. At present, it is imperative to identify a treatment to address the devastating post-TBI consequences. Therefore, the present study has been performed to assess the specific effect of immediate exposure to normabaric hyperoxia (NBO) after fluid percussion injury (FPI) in the striatum of mice. To execute FPI, mice were anesthetised and sorted into (i) a TBI group, (ii) a sham group without injury and (iii) a TBI group treated with immediate exposure to NBO for 3 h. Afterwards, brains were harvested for morphological assessment. The results revealed no changes in morphological and neuronal damage in the sham group as compared to the TBI group. Conversely, the TBI group showed severe morphological changes as well as neuronal damage as compared to the TBI group exposed to NBO for 3 h. Interestingly, our findings also suggested that NBO treatment could diminish the neuronal damage in the striatum of mice after FPI. Neuronal damage was evaluated at different points of injury and the neighbouring areas using morphology, neuronal apoptotic cell death and pan-neuronal markers to determine the complete neuronal structure. In conclusion, immediate exposure to NBO following FPI could be a potential therapeutic approach to reduce neuronal damage in the TBI model.
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Registered trials
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