Effects of Selective Cyclooxygenase-2 Inhibitor NS-398 Pretreatment on the Rat Spinal Cord after Contusion Injury.
- Author:
Hyeon Dae CHEONG
1
;
Joo Kyung SUNG
;
In Suk HAM
;
Ku Seong KANG
;
Joung Ok KIM
;
Jung Wan KIM
;
Tae In PARK
;
Yoon Kyung SOHN
Author Information
1. Department of Neurosurgery, Kyungpook National University School of Medicine, Daegu 700-422, Korea.
- Publication Type:Original Article
- Keywords:
Spinal cord injury;
Cyclooxygenase 2 inhibitors;
NS-398;
Cell death
- MeSH:
Animals;
Caspase 3;
Cell Death;
Contusions*;
Cyclooxygenase 2 Inhibitors;
Cyclooxygenase 2*;
Dinoprostone;
Fluorescence;
Microglia;
Neurons;
Rats*;
Spinal Cord Injuries;
Spinal Cord*
- From:Korean Journal of Pathology
2006;40(4):255-262
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Secondary spinal cord injury (SCI) that follows an initial mechanical insult can exacerbate the overall damage, limit the restorative processes and eventually lead to an in- creased neurological deficit. We hypothesized that selective inhibition of cyclooxygenase-2 (COX-2) may decrease the delayed cell death, and so this will contribute to decreased level of the secondary injury. METHODS: The dorsal surface of the cord at the T9 level was subjected to weight drop impact using a 10 g rod. To block COX-2 activation, a selective COX-2 inhibitor (NS-398) was administered (5 mg/kg, i.p.) 15 min prior to SCI. The COX-1, COX-2, Caspase-3 and PGE2 expressions were measured by real time quantitative RT-PCR and fluorescence immunostaining. RESULTS: Many activated caspase-3 positive cells were observed at 6 h and they increased until 72 h after SCI. The expression of COX-2 peaked at 6 h after SCI, while the COX-1 expression was unaffected. The principal cells that showed a COX-2 expression were the neurons and microglia. Pretreatment with NS-398 caused a significant decrease in the expression of prostaglandin E2 and activated caspase-3 positive cells after SCI. CONCLUSION: These data suggest that COX-2 is one of the main factors related with the pathologic deficits from secondary SCI.
