Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 27,971 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke.DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER, BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Thursday, March 28, 2019
Modified Citrus Pectin Prevents Blood-Brain Barrier Disruption in Mouse Subarachnoid Hemorrhage by Inhibiting Galectin-3
So you have identified a possible solution to a stroke problem. WHAT EXACTLY ARE YOU DOING TO GET THIS TO HUMAN CLINICAL TRIALS? Not doing anything is the height of incompetence and you, your mentors and senior researchers should all be fired. My vacations did not calm me down(Italy, London).
This from August 2015 should already have initiated human trials:
Plasma
levels of galectin-3—a matricellular protein—are increased after
aneurysmal subarachnoid hemorrhage (SAH), but the functional
significance remains undetermined. This study was conducted to evaluate
whether modified citrus pectin (MCP; galectin-3 inhibitor) prevents
post-SAH early brain injury, focusing on blood-brain barrier disruption.
Methods—
C57BL/6
male adult mice (n=251) underwent sham or filament perforation SAH
modeling, followed by a random intracerebroventricular injection of
vehicle or drug at 30 minutes post-modeling. First, vehicle-treated and
0.8, 4, 16, or 32 µg MCP-treated mice were assessed by neuroscore and
brain water content at 24 and 48 hours post-modeling. Second, Evans blue
extravasation, Western blotting, coimmunoprecipitation and
immunostaining were performed in vehicle-treated or 4 µg MCP-treated
mice at 24 hours post-modeling. Third, vehicle or R-galectin-3
(recombinant galectin-3) was administered to SAH mice simultaneously
with vehicle or MCP, and neuroscore and Evans blue extravasation were
evaluated at 24 hours post-modeling. Fourth, vehicle or R-galectin-3 was
administered to MCP-treated SAH mice at 24 hours, and neuroscore and
IgG immunostaining were evaluated at 48 hours post-SAH.
Results—
Among
tested dosages, 4 µg MCP showed the best neuroprotective effects as to
preventing neurological impairments and brain edema at 24 to 48 hours
post-SAH. Four micrograms MCP attenuated post-SAH blood-brain barrier
disruption and galectin-3 upregulation in brain capillary endothelial
cells, associated with inactivation of ERK (extracellular signal-related
kinase) 1/2, STAT (signal transducer and activator of transcription)-3,
and MMP (matrix metalloproteinase)-9, and the consequent preservation
of a tight junction protein ZO-1 (zonula occludens-1).
Coimmunoprecipitation assay demonstrated physical interactions between
galectin-3 and TLR (Toll-like receptor) 4. R-galectin-3 blocked the
neuroprotective effects of MCP.
Conclusions—
MCP
prevents post-SAH blood-brain barrier disruption possibly by inhibiting
galectin-3, of which the mechanisms may include binding to TLR4 and
activating ERK1/2, STAT-3, and MMP-9. This study suggests galectin-3 to
be a novel therapeutic target against post-SAH early brain injury.
Correspondence
to Hidenori Suzuki, MD, PhD, Department of Neurosurgery, Mie University
Graduate School of Medicine, 2–174 Edobashi, Tsu, Mie 514–8507, Japan.
Email suzuki02@clin.medic.mie-u.ac.jp
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