This was written about for stroke way back in 1998;
http://oc1dean.blogspot.com/2011/10/c-jun-transcription-factor-bipotential.html
Where the hell is the protocol to use this for stroke?
The newest article here:
http://www.alphagalileo.org/ViewItem.aspx?ItemId=128298&CultureCode=en
Using two different compounds they developed, scientists from the
Florida campus of The Scripps Research Institute (TSRI) have been able
to show in animal models that inhibiting a specific enzyme protects
heart cells and surrounding tissue against serious damage from heart
attacks. The compounds also protect against additional injury from
restored blood flow after an attack, a process known as reperfusion.
The study appears in the February 8, 2013 print edition of The Journal of Biological Chemistry.
A heart attack severely restricts blood supply, starving heart cells
and surrounding tissue of oxygen, which can cause enormous damage in
relatively little time—sometimes in just a few minutes. Known as an
ischemic cascade, this drop-off of oxygen results in a sudden crush of
metabolic waste that damages cell membranes as well as the mitochondria,
a part of the cell that generates chemical energy and is involved in
cell growth and death.
Unfortunately, restoring blood flow adds significantly to the damage,
a serious medical issue when it comes to treating major ischemic events
such as heart attack and stroke. Reperfusion re-invigorates production
of free radicals and reactive oxygen species that attack and damage
cells, exacerbating inflammation, turning loose white blood cells to
attack otherwise salvageable cells and maybe even inducing potentially
fatal cardiac arrhythmias.
The new study found that inhibiting the enzyme, c-jun-N-terminal
kinase (JNK), pronounced "junk," protected against ischemic/reperfusion
injury in rats, reducing the total volume of tissue death by as much as
34 percent. It also significantly reduced levels of reactive oxygen
species and mitochondrial dysfunction.
In earlier studies, TSRI scientists found that JNK migrates to the
mitochondria upon oxidative stress. That migration, coupled with JNK
activation, they found, is associated with a number of serious health
issues, including liver damage, neuronal cell death, stroke and heart
attack. The peptide and small molecule inhibitor (SR3306) developed by
LoGrasso and his colleagues blocks those harmful effects, thereby
reducing programmed cell death four-fold.
“This is the same story,” said Philip LoGrasso, a TSRI professor and
senior scientific director of discovery biology at Scripps Florida, who
led the study. “These just happen to be heart cells, but we know that
oxidative stress kills cells, and JNK inhibition protects against this
stress. Blocking the translocation of JNK to the mitochondria is
essential for stopping this killing cascade and may be an effective
treatment for damage done to heart cells during an ischemic/reperfusion
event.”
In addition, LoGrasso said, biomarkers that rise during a heart
attack shrink in the presence of JNK inhibition, a clear indication that
blocking JNK reduces the severity of the infarction.
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