Dados do Trabalho

Título

PRIOR NANDROLONE DECANOATE ADMINISTRATION ATTENUATES MITOCHONDRIAL DYSFUNCTION AND CELL DEATH AFTER TRAUMATIC BRAIN INJURY.

Fundamentação/Introdução

INTRODUCTION: Traumatic brain injury (TBI) causes neurodegeneration and cognitive impairment by mechanisms particularly associated with mitochondrial dysfunction and neuroenergetics deficits. Anabolic androgenic steroids (AAS), such as Nandrolone Decanoate (ND), are synthetic hormones derivatives of testosterone used to improve physical ability. Professional athletes are frequently users of AAS and have a high risk of suffering from repeated TBI during their careers. TBI therapy in general is still challenging and there is no specific therapy available to target mitochondrial dysfunction triggered by TBI.

Objetivos

Investigate the effects of ND administration prior to TBI on memory and mitochondrial bioenergetics.

Delineamento e Métodos

METHODS: we performed an experimental study where male 60 days old CF1 mice were treated with ND 15mg/kg or vehicle (VEH) subcutaneously for 19 days. Posterior to treatment, the animals were submitted to a craniotomy followed by a moderate cortical controlled impact, thus being divided into four distinct groups: VEH/SHAM, ND/SHAM, VEH/CCI and ND/CCI. After 48 h rest animals were evaluated for cognitive function through five days Morris Water Maze task (MWM). After that, synaptosomes of the ipsilateral hemisphere were used to analyze mitochondrial metabolism through respirometry, H2O2 production and mitochondrial membrane potential (∆Ѱm). Cellular viability was investigated by MTT assay. Data was analyzed using One Way ANOVA, followed by Tukey post hoc. Statistical significance was considered when p<0.05.

Resultados

RESULTS: CCI impaired spatial memory, increased H2O2 production, disturbed ∆Ѱm formation resulting in decreased cell viability seven days after a moderate TBI. ND administration prior to TBI attenuated the spatial memory deficits, and decreased H2O2 production, ∆Ѱm and sustained cell viability. Remarkably.

Conclusões/Considerações Finais

CONCLUSION: ND seems to exert a preventive benefit to brain mitochondrial neuroenergetics function and cell survival in mice submitted to TBI. In our concept, our data highlights the potential relevance of AAS as neuroprotective agents for TBI therapy.

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Palavras-chave

KEY WORDS: Traumatic Brain Injury, Anabolic Androgen Steroids, Cognition, Mitochondrial Function