You just might want your doctor and hospital to contact researchers to follow this up with human testing for the improvement neurogenesis. Up to you, YOUR HOSPITAL WILL DO NOTHING WITHOUT YOUR PRODDING.
Intraventricular Medium B Treatment Benefits an Ischemic Stroke Rodent Model via Enhancement of Neurogenesis and Anti-apoptosis
Abstract
Enhancement
of endogenous neurogenesis after ischemic stroke may improve functional
recovery. We previously demonstrated that medium B, which is a
combination with epidermal growth factor (EGF) and fibronectin, can
promote neural stem/progenitor cell (NSPC) proliferation and migration.
Here, we showed that medium B promoted proliferation and migration of
cultured NSPCs onto various 3-dimentional structures. When rat cortical
neurons with oxygen glucose deprivation (OGD) were co-cultured with
NSPCs, medium B treatment increased neuronal viability and reduced cell
apoptosis. In a rat model with transient middle cerebral artery
occlusion (MCAO), post-insult intraventricular medium B treatment
enhanced proliferation, migration, and neuronal differentiation of NSPCs
and diminished cell apoptosis in the infarct brain. In cultured
post-OGD neuronal cells and the infarct brain from MCAO rats, medium B
treatment increased protein levels of Bcl-xL, Bcl-2, phospho-Akt,
phospho-GSK-3β, and β-catenin and decreased the cleaved caspase-3 level,
which may be associated with the effects of anti-apoptosis. Notably,
intraventricular medium B treatment increased neuronal density, improved
motor function and reduced infarct size in MCAO rats. In summary,
medium B treatment results in less neuronal death and better functional
outcome in both cellular and rodent models of ischemic stroke, probably
via promotion of neurogenesis and reduction of apoptosis.
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