Effect of selective inhibition of cyclooxygenase 2 on temporary focal cerebral ischemia in rats

Kazushi Hara; Daniel L. Kong; Frank R Sharp; Philip R. Weinstein

doi:10.1016/S0304-3940(98)00755-1

Effect of selective inhibition of cyclooxygenase 2 on temporary focal cerebral ischemia in rats

Kazushi Hara, Daniel L. Kong, Frank R Sharp, Philip R. Weinstein

Research output: Contribution to journal › Article › peer-review

47 Scopus citations

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	https://doi.org/10.1016/S0304-3940(98)00755-1
State	Published - Oct 30 1998
Externally published	Yes

Keywords

Brain
Cyclooxygenase 2
Ischemia
NS-398
Prostaglandin E2
Rat

ASJC Scopus subject areas

Neuroscience(all)

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10.1016/S0304-3940(98)00755-1

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title = "Effect of selective inhibition of cyclooxygenase 2 on temporary focal cerebral ischemia in rats",

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.",

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AU - Hara, Kazushi

AU - Kong, Daniel L.

AU - Sharp, Frank R

AU - Weinstein, Philip R.

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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.

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