WHOM will your doctor contact to get this tested for stroke in humans? No contact then you need to have that doctor fired for incompetency and dereliction of duty. We need to start clearing out a lot of dead wood in stroke, probably starting with your stroke hospital board of directors. And it is for hyperacute with a delayed time frame, so every survivor could get it.
ApoA-I Mimetic Peptide Reduces Vascular and White Matter Damage After Stroke in Type-2 Diabetic Mice
- 1Department of Neurology, Henry Ford Hospital, Detroit, MI, United States
- 2Department of Physics, Oakland University, Rochester, MI, United States
Diabetes leads to an elevated risk of stroke and worse
functional outcome compared to the general population. We investigate
whether L-4F, an economical ApoA-I mimetic peptide, reduces
neurovascular and white-matter damage in db/db type-2 diabetic (T2DM)
stroke mice. L-4F (16 mg/kg, subcutaneously administered initially 2 h
after stroke and subsequently daily for 4 days) reduced hemorrhagic
transformation, decreased infarct-volume and mortality, and treated mice
exhibited increased cerebral arteriole diameter and smooth muscle cell
number, decreased blood-brain barrier leakage and white-matter damage in
the ischemic brain as well as improved neurological functional outcome
after stroke compared with vehicle-control T2DM mice (p < 0.05, n
= 11/group). Moreover, administration of L-4F mitigated macrophage
infiltration, and reduced the level of proinflammatory mediators tumor
necrosis factor alpha (TNFα), high-mobility group box-1
(HMGB-1)/advanced glycation end-product receptor (RAGE) and plasminogen
activator inhibitor-1 (PAI-1) in the ischemic brain in T2DM mice (p < 0.05, n = 6/group). In vitro,
L-4F treatment did not increase capillary-like tube formation in
mouse-brain endothelial cells, but increased primary artery explant cell
migration derived from C57BL/6-aorta 1 day after middle cerebral artery
occlusion (MCAo), and enhanced neurite-outgrowth after 2 h of
oxygen-glucose deprivation and axonal-outgrowth in primary cortical
neurons derived from the C57BL/6-embryos subjected to high-glucose
condition. This study suggests that early treatment with L-4F provides a
potential strategy to reduce neuroinflammation and vascular and
white-matter damage in the T2DM stroke population.
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