RT Journal Article
SR Electronic
T1 Which is more effective in reducing secondary brain damage resulting from cyclooxygenase expression following traumatic brain injury: calcium channel blockers or cox inhibitors?
JF Neurosciences Journal
JO Neurosciences (Riyadh)
FD Prince Sultan Military Medical City
SP 239
OP 243
VO 13
IS 3
A1 Karabekir, Hamit S.
A1 Balci, Canan
A1 Aktepe, Fatma
A1 Tokyol, Cigdem
A1 Dilek, Husniye
YR 2008
UL http://nsj.org.sa/content/13/3/239.abstract
AB OBJECTIVE: 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. METHODS: 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.RESULTS: 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.CONCLUSION: 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.