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.