Abstract
Small Rho GTPases act through the Rho-associated kinase (ROCK) activated by them, and control the migration, proliferation and death of neural cells and reactive astrogliosis. The Rho/ROCK signal pathway mediates the effect of endogenous axons growth inhibitors from myelin, oligodendrocytes and glial scar and it is activated in spinal cord trauma, which leads to an increased inflammatory response, neuropathic pain, demyelination, cell death, inhibition of axon growth, and impaired function. After spinal cord injury under conditions of pharmacological inhibition of Rho/ROCK was shown increased level of growth and branching, increased plasticity of neuronal structures and intercellular communications, neuroprotective effect, increased remyelinization and improved function. In addition to selective inhibitors of RhoA (ADP-ribosyltransferase C3) and ROCK (Fasudil, Y-27632 and Y-39983), the ability to inhibit Rho/ROCK was indicated for non-steroidal anti-inflammatory drugs such as ibuprofen and indomethacin, as well as for statins.
Published Version
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