Iron Collecting Antibiotic In Stroke

[ironjustice]

Antibiotic studied to reduce hemorrhagic stroke damage

http://medicalxpress.com/news/2013-04-antibiotic-hemorrhagic.html

April 1, 2013 in Cardiology

This is Dr. Jeffrey A. Switzer, stroke specialist at the Medical
College of Georgia at Georgia Regents University, and Dr. Susan C.
Fagan, Assistant Dean of the University of Georgia College of
Pharmacy. Credit: Phil Jones

A new study will help determine if an antibiotic is a partial antidote
for the poisonous effect blood has on the brain following a
hemorrhagic stroke, researchers say.

They want to know if minocycline, a broad-spectrum antibiotic, can
reduce high rates of disability from this comparatively rare stroke
type characterized by spontaneous bleeds into the brain, said Dr.
Jeffrey A. Switzer, stroke specialist at the Medical College of
Georgia at Georgia Regents University.

"We hope that, given early, minocycline can help reduce the damage of
a type of stroke for which there is currently no proven therapy,"
Switzer said. He is principal investigator on an American Heart
Association grant funding a trial enrolling 24 patients over two
years, half of whom will get minocycline.

Dr. David Hess, Chair of the MCG Department of Neurology, and Dr.
Susan C. Fagan, Assistant Dean of the University of Georgia College of
Pharmacy, have shown minocycline is safe and potentially effective at
combating some collateral damage of the more common clot-based
strokes.

In a follow-up analysis, minocycline also appeared to reduce the
inflammation that follows the initial stroke as well as levels of
matrix metalloproteinases, or MMPs, a family of enzymes that destroys
the basement membrane of blood vessels, making rupture more likely.

Elevated levels of MMPs and inflammatory cells have been found in the
blood of both kinds of stroke patients and high levels correlate with
poor outcomes. Minocycline also is known as a powerful collector of
iron, a vital blood component that helps transport oxygen inside blood
vessels but poisons brain tissue upon direct contact.

Switzer hopes minocycline will reduce levels of all three in
hemorrhagic stroke, reducing bleeding and the size and impact of the
stroke. Nearly 40 percent of hemorrhagic strokes increase in size
during the first 24 hours. Most of the growth occurs within the first
few hours, so timely intervention could reduce brain tissue loss, he
said.

In fact, if minocycline proves safe in hemorrhagic strokes, the
researchers believe the best place to give it would be in an ambulance
on the way to the hospital. Minocycline may be able to expand the
window during which the clot buster tPA can be given to ischemic
stroke patients. Switzer and his colleagues have first-hand experience
that the earlier the better with stroke intervention. "If we could
give something in the field before we can confirm the type of stroke
because we know it's safe for both, that would be a novel strategy to
help patients," he said.

For the study, they will use computerized tomography, or CT, to
confirm a hemorrhagic stroke then get baseline assessments of blood
levels of agents of interest, such as MMPs, as well as the patient's
cognitive and physical abilities before giving the first dose of
minocycline intravenously. Subsequent doses will be given orally, if
the patient can swallow, over the next four days. Measures of outcomes
and biomarkers will be reassessed at 24 hours, seven days or at time
of hospital discharge and again at 90 days post-stroke.

They hope that decreasing blood levels of MMPs will serve as an
indicator of how well the therapy works.

Risk factors for hemorrhagic stroke include uncontrolled hypertension;
use of older blood thinners commonly prescribed for conditions such as
heart disease and clots in the legs; and amyloid angiopathy, a deposit
of Alzheimer's-like plaque that weakens the walls of blood vessels on
the brain surface, typically in older individuals.

In addition to the substances in the blood that do harm, the physical
mass created by bleeding causes damage. "It's tearing and pushing on
structures in the brain and can cause a shifting of tissue that can be
fatal in the closed chamber of the skull," Switzer said. "However, for
those with smaller bleeds, better treatments, such as perhaps
minocycline, are needed to combat the toxic effects of blood on brain
tissue."


Provided by Medical College of Georgia


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[ironjustice]

On Apr 2, 7:22 am, ironjustice <ironjust...@cool.zzn.com> wrote: a
powerful collector of iron <<

"Iron chelator, deferoxamine, attenuated the ICH"

DARPP-32 to quantify intracerebral hemorrhage-induced neuronal death
in basal ganglia.
Jin H, Xi G, Hua Y
Stroke Res 2013 Feb 1; 4(1):130-134
Abstract
Quantification of acute brain injury in basal ganglia is essential for
mechanistic and therapeutic studies in experimental intracerebral
hemorrhage (ICH).
Using conventional counting of degenerating cells based on
morphological or immunohistochemical criteria, it is hard to define
the boundary of the whole lesion area.
Dopamine- and cAMP-regulated phosphoprotein, Mr 32 kDa (DARPP-32) is a
cytosolic protein highly enriched in medium-sized spiny neurons of the
striatum.
We developed new methods for quantifying lesion area by detecting the
difference of the DARPP-32 negative area and the hematoma clot, and by
measuring DARPP-32 protein level for semi-qualification in rat model
of ICH.
We found that DARPP-32 negative area around hematoma was present at
day-1, peaked at day-3, and decreased at day-14 after ICH, a time
course paralleled by DARPP-32 Western blots.
The DARPP-32 negative area matched well with the necrotic area
determined using propidium iodide.
Treatment with an iron chelator, deferoxamine, attenuated the ICH-
induced reduction in DARPP-32 protein levels.
These results suggest that DARPP-32 is a simple and quantifiable
indicator of ICH-induced neuronal death in basal ganglia.