Which is more effective in reducing secondary brain damage resulting from cyclooxygenase expression following traumatic brain injury: calcium channel blockers or cox inhibitors?

ABSTRACT

To evaluate localizations of cyclooxygenase [COX]-1 and COX-2 following traumatic brain injury [TBI] and the effects of 2 therapeutic agents on COX inhibition. Forty rabbits were used in this study for developing a TBI model and divided into 4 groups [n=10] at Afyon Kocatepe University School of Medicine, Afyonkarahisar, Turkey in June 2004. Differential cellular COX-1 and COX-2 protein expression profiles were analyzed following TBI, and the effects of 2 therapeutic agents, indomethacin and nimodipine, on COX inhibition were evaluated immunohistochemically. This study revealed that COX-1 and COX-2 protein expression were significantly increased in vascular endothelial, smooth muscle cells, and CD68+ microglia/macrophages following TBI. Indomethacin inhibited the COX expression in glial cells more than nimodipine, however, both did not affect endothelial COX-1 and COX-2 expression. The restricted accumulation of COX-1 at the perilesional area points to an acute inflammatory response and the role of COX-1 in TBI. This study revealed that COX-1 expression should be a pharmacological target following TBI, and COX-2 should also be evaluated in this aspect, and indomethacin is more effective than nimodipine for blocking COX-1