NSAID ibuprofen

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RhoA-inhibiting NSAIDs promote axonal myelination after spinal cord injury.

Exp Neurol. <http://www.ncbi.nlm.nih.gov/pubmed/21781963> 2011

Oct;231(2):247-60. Epub 2011 Jul 14.

http://www.ncbi.nlm.nih.gov/pubmed/21781963

Abstract

Nonsteroidal anti-inflammatory drugs (NSAIDs) are extensively used to

relieve pain and inflammation in humans via cyclooxygenase inhibition. Our

recent research suggests that certain NSAIDs including ibuprofen suppress

intracellular RhoA signal and improve significant axonal growth and

functional recovery following axonal injury in the CNS. Several NSAIDs have

been shown to reduce generation of amyloid-beta42 peptide via inactivation

of RhoA signal, supporting potent RhoA-repressing function of selected

NSAIDs. In this report, we demonstrate that RhoA-inhibiting NSAIDs ibuprofen

and indomethacin dramatically reduce cell death of oligodendrocytes in

cultures or along the white matter tracts in rats with a spinal cord injury.

More importantly, we demonstrate that treatments with the RhoA-inhibiting

NSAIDs significantly increase axonal myelination along the white matter

tracts following a traumatic contusion spinal cord injury. In contrast,

non-RhoA-inhibiting NSAID naproxen does not have such an effect. Thus, our

results suggest that RhoA inactivation with certain NSAIDs benefits recovery

of injured CNS axons not only by promoting axonal elongation, but by

enhancing glial survival and axonal myelination along the disrupted axonal

tracts. This study, together with previous reports, supports that RhoA

signal is an important therapeutic target for promoting recovery of injured

CNS and that RhoA-inhibiting NSAIDs provide great therapeutic potential for

CNS axonal injuries in adult mammals.

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