Deans' stroke musings: Mn (III) tetrakis (4-Benzoic Acid) porphyrin scavenges reactive species, reduces oxidative stres s, and improves functional recovery after experimental spinal cord injury in rats: comparison with methylprednisolone

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Tuesday, March 5, 2013

Mn (III) tetrakis (4-Benzoic Acid) porphyrin scavenges reactive species, reduces oxidative stres s, and improves functional recovery after experimental spinal cord injury in rats: comparison with methylprednisolone

Ask your doctor why this wouldn't help in stroke recovery. And then ask when s/he is going to start clinical trials on this.
http://www.biomedcentral.com/content/pdf/1471-2202-14-23.pdf

Abstract

Background

Substantial experimental evidence supports that reactive species mediate secondary damage

after traumatic spinal cord injury (SCI) by inducing oxidative stress. Removal of reactive

species may reduce secondary damage following SCI. This study explored the effectiveness

of a catalytic antioxidant - Mn (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP) - in

removing reactive oxygen species (ROS), reducing oxidative stress, and improving functional

recovery in vivo in a rat impact SCI model. The efficiency of MnTBAP was also compared

with that of methylprednisolone – the only drug used clinically in treating acute S

CI.

Results

In vivo measurements of time courses of ROS production by microdialysi

s and microcannula sampling in MnTBAP, methylprednisolone, and saline (as vehicle contr

ol)-treated SCI rats showed that both agents significantly reduced the production of hydrogen

peroxide, but only MnTBAP significantly reduced superoxide elevation after SCI.

In vitro experiments further demonstrated that MnTBAP scavenged both of the preceding ROS, whereas methylprednisolone had no effect on either. By counting the immuno-positive

neurons in the spinal cord sections immunohistochemically stained with anti-nitrotyrosine and anti-4-hydroxy-nonenal antibodies as the markers of protein nitration and membrane lipid peroxidation, we demonstrated that MnTBAP significantly reduced the numbers of 4-hydroxy-nonenal-positive and nitrotyrosine-positive neurons in the sections at 1.55 to 2.55 mm and 1.1 to 3.1 mm, respectively, rostral to the injury epicenter compared to the vehicle-treated animals. By behavioral tests (open field and inclined plane tests), we demonstrated that at 4 hours post-SCI treatment with MnTBAP and the standard met hylprednisolone regimen both significantly increased test scores compared to thos

e produced by vehicle treatment. However, the outcomes for MnTBAP-treated rats were significantly better than those for methylprednisolone-treated animals.

Conclusions

This study demonstrated for the first time in vivo and in vitro that MnTBAP significantly reduced the levels of SCI-elevated ROS and that MnTBAP is superior to methylprednisolone in removing ROS. Removal of ROS by MnTBAP significantly reduced protein nitration and membrane lipid peroxidation in neurons. MnTBAP more effectively reduced neurological deficits than did by methylprednisolone after SCI - the first most important criterion for assessing SCI treatments. These results support the therapeutic potential of MnTBAP in treating SCI.