http://www.sciencedirect.com/science/article/pii/S0306452213005472
Highlights
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- Exercise facilitates the action of DHA in preserving DHA homeostasis after TBI.
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- Exercise enhances the effects of DHA on counteracting the outcome of TBI.
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- These findings may have important therapeutic potential for the treatment of TBI.
Abstract
The
abilities of docosahexaenoic acid (DHA) and exercise to counteract
cognitive decay after TBI is getting increasing recognition; however,
the possibility that these actions can be complementary remains just as
an intriguing possibility. Here we have examined the likelihood that the
combination of diet and exercise has the added potential to facilitate
functional recovery following TBI. Rats received mild fluid percussion
injury (mFPI) or sham injury and then were maintained on a diet high in
DHA (1.2% DHA) with or without voluntary exercise for 12 days.
We found
that FPI reduced DHA content in the brain, which was accompanied by
increased levels of lipid peroxidation assessed using 4-HHE. FPI reduced
the enzymes Acox1 and 17β-HSD4, and the calcium-independent
phospholipases A2 (iPLA2), which are involved in metabolism
of membrane phospholipids. FPI reduced levels of syntaxin-3 (STX-3),
involved in the action of membrane DHA on synaptic membrane expansion,
and also reduced BDNF signaling through its TrkB receptor.
These effects
of FPI were optimally counteracted by the combination of DHA and
exercise. Our results support the possibility that the complementary
action of exercise is exerted on restoring membrane homeostasis after
TBI, which is necessary for supporting synaptic plasticity and
cognition. It is our contention that strategies that take advantage of
the combined applications of diet and exercise may have additional
effects to the injured brain.
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