Abstract
Cyclooxygenase 2 (COX2) is the inducible isoform of COX but its involvement in ischemic neuronal injury is unclear. The effect of selective inhibition of COX2 was evaluated by intraperitoneal administration of NS- 398, a selective COX2 inhibitor, before and after 2 h of temporary focal ischemia in rats. After 4 h of reperfusion, the infarct volume and the hemispheric concentration of prostaglandin E2 (PGE2), a major substance produced by COX2, were assessed. The infarct volume was unchanged by NS-398 administration. There was no difference in PGE2 levels between the ischemic and the contralateral hemispheres in the control group. However, PGE2 concentration significantly decreased in the ischemic hemisphere in the NS- 398 group. The results are consistent with the previous observation that COX2 is induced in peri-ischemic areas and suggests that COX2 has a significant role in peri-ischemic pathophysiology.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 53-56 |
| Number of pages | 4 |
| Journal | Neuroscience Letters |
| Volume | 256 |
| Issue number | 1 |
| DOIs | |
| State | Published - Oct 30 1998 |
| Externally published | Yes |
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Keywords
- Brain
- Cyclooxygenase 2
- Ischemia
- NS-398
- Prostaglandin E2
- Rat
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Effect of selective inhibition of cyclooxygenase 2 on temporary focal cerebral ischemia in rats. / Hara, Kazushi; Kong, Daniel L.; Sharp, Frank R; Weinstein, Philip R.
In: Neuroscience Letters, Vol. 256, No. 1, 30.10.1998, p. 53-56.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Effect of selective inhibition of cyclooxygenase 2 on temporary focal cerebral ischemia in rats
AU - Hara, Kazushi
AU - Kong, Daniel L.
AU - Sharp, Frank R
AU - Weinstein, Philip R.
PY - 1998/10/30
Y1 - 1998/10/30
N2 - Cyclooxygenase 2 (COX2) is the inducible isoform of COX but its involvement in ischemic neuronal injury is unclear. The effect of selective inhibition of COX2 was evaluated by intraperitoneal administration of NS- 398, a selective COX2 inhibitor, before and after 2 h of temporary focal ischemia in rats. After 4 h of reperfusion, the infarct volume and the hemispheric concentration of prostaglandin E2 (PGE2), a major substance produced by COX2, were assessed. The infarct volume was unchanged by NS-398 administration. There was no difference in PGE2 levels between the ischemic and the contralateral hemispheres in the control group. However, PGE2 concentration significantly decreased in the ischemic hemisphere in the NS- 398 group. The results are consistent with the previous observation that COX2 is induced in peri-ischemic areas and suggests that COX2 has a significant role in peri-ischemic pathophysiology.
AB - Cyclooxygenase 2 (COX2) is the inducible isoform of COX but its involvement in ischemic neuronal injury is unclear. The effect of selective inhibition of COX2 was evaluated by intraperitoneal administration of NS- 398, a selective COX2 inhibitor, before and after 2 h of temporary focal ischemia in rats. After 4 h of reperfusion, the infarct volume and the hemispheric concentration of prostaglandin E2 (PGE2), a major substance produced by COX2, were assessed. The infarct volume was unchanged by NS-398 administration. There was no difference in PGE2 levels between the ischemic and the contralateral hemispheres in the control group. However, PGE2 concentration significantly decreased in the ischemic hemisphere in the NS- 398 group. The results are consistent with the previous observation that COX2 is induced in peri-ischemic areas and suggests that COX2 has a significant role in peri-ischemic pathophysiology.
KW - Brain
KW - Cyclooxygenase 2
KW - Ischemia
KW - NS-398
KW - Prostaglandin E2
KW - Rat
UR - http://www.scopus.com/inward/record.url?scp=0032582614&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0032582614&partnerID=8YFLogxK
U2 - 10.1016/S0304-3940(98)00755-1
DO - 10.1016/S0304-3940(98)00755-1
M3 - Article
C2 - 9832215
AN - SCOPUS:0032582614
VL - 256
SP - 53
EP - 56
JO - Neuroscience Letters
JF - Neuroscience Letters
SN - 0304-3940
IS - 1
ER -