Indomethacin protects rats from neuronal damage induced by traumatic brain injury and suppresses hippocampal IL-1β release through the inhibition of Nogo-A expression

Background: 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 (tbi)-induced inflammation and neuronal damage.methods: a weight-drop device was used to deliver a standard traumatic impact to rats. western blot,rt-pcr and elisa were used to analyze the expression of nogo-a and il-1β. nogo-a antisense,and an irrelevant control oligonucleotide was intracerebroventricularly infused. we also performed h & e staining and luxol fast blue staining to evaluate the neuronal damage and demyelination resulting from tbi and various treatments.results: based on rt-pcr and western blot analyses,the expression of nogo-a was found to be significantly upregulated in the hippocampus beginning eight hours after tbi. in addition,tbi caused an apparent elevation in il-1β levels and severe neuronal damage and demyelination in the tested animals. all of the tbi-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 specific nogo-a antisense oligonucleotide.conclusions: our findings suggest that the suppression of nogo-a expression appears to be an early response conferred by indomethacin,which then leads to decreases in the levels of il-1β and tbi-induced neuron damage. © 2012 chao et al.; licensee biomed central ltd.