Nogo-A is a member of the reticulon family of membrane-associated proteins and plays an important role in axonal remodeling.The present study aimed to investigate alterations in Nogo-A expression following traumatic brain injury (TBl)-induced inflammation and neuronal damage.Based on RT-PCR and western blot analyses, the expression of Nogo-A was found to be significantly upregulated in the hippocampus starting at eight hours after TBI.In addition, TBI caused an apparent elevation in IL-1β levels, severe neuronal damage,and demyelination in the tested animals.All these TBl-associated molecular and cellular consequences could be effectively reversed by treating the animals with the anti-inflammatory drug indomethacin.More importantly, the TBI-associated stimulation in the levels of both Nogo-A and IL-1β could be effectively inhibited by a specifc Nogo-A antisense oligonucleotide.Our findings suggest that the suppression of Nogo-A expression appears to be an early response conferred by indomethacin, which in turn leads to the subsidence in the levels of IL-1 β and TBIinduced neuron damage.