Your doctor should be able to hypothesize a stroke protocol from this and contact his research team to setup clinical trials. Its so damn obvious and I don't want to wait 30 years before someone else thinks of this. Why am I not in charge?
Alpha tocopherol treatment reduces the expression of Nogo-A and NgR in rat brain after traumatic brain injury
Abstract
Background
Neurite
outgrowth inhibitor-A (Nogo-A), myelin-associated glycoprotein, and
oligodendrocyte myelin glycoprotein are three myelin-associated proteins
that act as inhibitors to central nervous system regeneration. Neurite
outgrowth inhibitor-A imposes the strongest effect on inhibiting axonal
regeneration after traumatic brain injury. Alpha-tocopherol, a member of
the vitamin E family, is recognized as an active antioxidative
substance. Its use has not been well studied in brain injury research,
especially in axonal regeneration research.
Methods
We
obtained 99 intact adult male Sprague–Dawley rats (200–250 g) from the
Experimental Animal Center of Central South University. We used the
modified method of Freeney to generate moderate brain injury in the
rats. We injected 600 mg/kg α-tocopherol intraperitoneally daily as
traumatic brain injury (TBI) treatment. Then, we performed behavioral
tests in the corresponding time point, examined brain tissues after
hematoxylin-eosin staining to identify changes in cell morphology, and
performed immunohistochemical staining and quantitative real-time
polymerase chain reaction to detect the expression of NoGo and Nogo
receptor (NgR) in brain tissue.
Results
For
the Neurological Severity Scores of rats, there were obvious
differences among the three groups at the corresponding time points.
Standard hematoxylin-eosin staining showed that the brain structure of a
sham-operated group of rats was clear, uniform, and compact. A TBI
group exhibited hemorrhage, edema, inflammatory cell infiltration,
condensed nuclei, and necrosis. We also saw glial cells and fibrous
tissue proliferation. The α-tocopherol–treated TBI group had similar but
less severe changes than the TBI group. Expression of Nogo-A and NgR
increased after TBI compared with the sham-operated group. However,
Nogo-A and NgR expression was significantly lower in the
α-tocopherol–treated TBI group compared with the TBI group. Similarly,
results showed that functional neurological deficits among rats in the
α-tocopherol–treated TBI group were less pronounced than in the TBI
group (model group).
Conclusions
Our
data demonstrate that α-tocopherol–treated rats had reduced microscopic
evidence of brain damage. Alpha-tocopherol reduced Nogo-A and NgR
expression in brain tissue after traumatic brain injury and promoted
nerve regeneration. Alpha-tocopherol treatment of TBI rats had a
neuroprotective role in their recovery.
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