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The influence of traumatic brain injury and ethyl pyruvate treatment on the neuronal
cytoskeleton

Anja Todorović
Regional center for talented youth Belgrade II, anjatodorovic97@gmail.com
surgery, and this group was also divided into two
Introduction subgroups: a) animals treated with saline solution once a
day during 2 days; b) animals treated with saline solution
once a day during 7 days. The third group consisted of
Traumatic injuries of the central nervous system (brain and
spinal cord) are one of the leading causes of death and intact animals that were used as a physiological control and
disability in an enormous number of people in the world that didn’t suffer the brain injury. The fourth group
and this number only increases through time. The working- consisted of intact animals treated with EP.
age population (20-50 years of age) is particularly affected As an experimental animal model of TBI, a puncture injury
by this phenomenon. The most common causes of these in the region of the right sensomotor cortex (2 mm behind
injuries are traffic incidents, work-related injuries and sport bregma, 2 mm lateral from the sagittal structure, 2 mm in
injuries. Traumatic brain injury (TBI) can cause cognitive depth) was used. The animals were anesthetized with ether
and neurological problems, which can appear right after the before the operation. The EP treatment (125 mg/kg of body
injury, but which can also develop and transform over time. weight) was initiated 60 min. after the operation and the
Unfortunately, there are still no adequate therapeutic protocol was applied once a day during 2 and 7 days. As a
approaches in preventing these consequences, therefore the marker for the dendrite extensions of neurons MAP2 was
primary goal of science is to discover the most effective used, for the neuron bodies NeuN, for the neuronal fibers
methods which would be used to improve the health Neurofilament 200, and for neurogenesis DCX. The
condition of the injured people. In order to understand the neurons which were in process of neurodegeneration were
brain injury pathology, a brain injury division was made, identified with the fluorescent color Fluoro-Jade B.
and it was divided into primary and secondary injury. The
damage created as a result of the initial mechanical event
represents a primary injury which is irreversible. The Results and discussion
secondary injury represents an assembly of biochemical and
metabolic changes initiated by the mechanical injury and it Immunohistochemical and double-immunofluorescent
leads to the dying away of neurons in the zones that are not staining showed that the injury leads to neurodegeneration
directly affected by the lesion after the TBI and it continues in the region around the lesion, which is particularly
in the following days, and even weeks. As a result of the expressed in day 7. Not only did the ethyl pyruvate
brain trauma it comes to the damaging of cytoskeletal treatment prevent the neurodegeneration, but it also
elements of the neurons which is one of the causes of their stimulated ramification of neurons around the lesion. The
disfunction. In this paper, it was examined how the brain treatment also increased the number of migrating immature
injury affects the expression of the main cytoskeletal neurons, in the subventricular zone of the lateral brain
proteins of neurons: neurofilaments, a protein attached to ventricule and gyrus dentatus of the hippocampus (which
the microtubules (Microtubule Associated Protein, MAP2) represent the main places of neurogenesis in an adult brain),
and a protein doublecortin (DCX) which is necessary for but also in the place of the injury itself.
the normal migration of neurons into the cerebral cortex.
The influence of the ethyl pyruvate treatment (EP) on the Conclusion
recovery processes after TBI was monitored The results have showed for the first time that ethyl
simultaneously. The pyruvate represents a key point for pyruvate treatment increases the expression of cytoskeletal
several metabolic pathways, and EP is its derivative that proteins in neurons, and that it also incites the processes of
has been shown to not only increases the metabolism, but it neurogenesis, therefore the ethyl pyruvate treatment could
is also a strong antioxidant, it prevents neuroimflammation be effective in brain injury therapy.
and apoptosis, and has a neuroprotective effect. The aim of
this paper was to examine the influence of the ethyl
pyruvate treatment on the cytoskeletal structures of Literature
neurons.
Maas A.I.R. et al. (2008). Moderate and severe traumatic
brain injury in adults. The Lancet Neurology. p. 728–741.
Materials and methods Moro N. et al. (2010). Beneficial Effects of Sodium or

Ethyl Pyruvate after Traumatic Brain Injury in the Rat.
In the experiment, male Wistar rats of approximately 75 Experimental Neurology. 225(2): 391–401.
days of age and body mass 200-250 g were used. The first
group consisted of animals that have gone through the Shi H. et al. (2014). Ethyl Pyruvate Protects against Blood–
surgery and suffered an injury of the left sensomotor cortex. Brain Barrier Damage and Improves Long-term
This group was divided into two subgroups: a) animals Neurological Outcomes in a Rat Model of Traumatic Brain
treated with EP once a day during 2 days; b) animals treated Injury. CNS Neuroscience & Therapeutics. doi:
with EP once a day during 7 days. The second group 10.1111/cns.12366
(Sham) consisted of animals that have gone through