Induction of cyclooxygenase-2 mRNA in gerbil hippocampal neurons after transient forebrain ischemia

Ohtsuki, T.

doi:10.1016/s0006-8993(96)00948-1

Cited by 27 publications

(45 citation statements)

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“…In rodents, as well as humans, cerebral ischemia up-regulates COX-2 expression in neurons, blood vessels, and inflammatory cells in the injured brain (42,43). Therefore, the administration of a selective COX-2 inhibitor attenuated the elevation of PGE 2 and reduced the infarct in a model of MCAO (15).…”

Section: Discussionmentioning

confidence: 99%

Panax notoginseng Attenuates the Infarct Volume in Rat Ischemic Brain and the Inflammatory Response of Microglia

et al. 2009

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Abstract. The roots of Panax notoginseng (PN) are commonly used as a therapeutic agent to stop hemorrhage and as a tonic to promote health in traditional Korean medicine. Stroke triggers an inflammatory response that not only plays a central role in the pathogenesis of cerebral ischemia, but also induces secondary damage. This study was designed to investigate the neuroprotective effects of the methanol extract of PN on the infarct volume induced by middle cerebral artery occlusion (MCAO) (90-min occlusion and 24-h reperfusion) in rat brains. The PN extract (50 mg/ kg, i.p.) was administered 2 h after the onset of MCAO. The PN-treated groups had a reduction in infarct volume by 23.82 ± 8.9%. In the PN extract-treated groups, the microglial density was significantly decreased in the peri-infarct region; the underlying mechanism was inhibition of inflammatory mediators, such as inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, via blocking of the NF-κB pathway. Furthermore, in vitro studies showed that the PN extract significantly reduced the production of iNOS-derived NO and COX-2-derived prostaglandin E 2 through the regulation of gene transcription levels in primary microglia and BV-2 cells. These results suggest that anti-inflammatory and microglial activation inhibitory effects of the PN extract may contribute to its neuroprotective effects in brain ischemia.

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Section: Discussionmentioning

confidence: 99%

Panax notoginseng Attenuates the Infarct Volume in Rat Ischemic Brain and the Inflammatory Response of Microglia

et al. 2009

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“…Whereas resuscitative efforts often restore perfusion to the brain, still a considerable number of patients end up having permanent cerebral damage because only minutes of global ischemia can lead to permanent brain injury (Petito et al, 1987). Thus, if nimesulide proves as protective in humans as in rodents, resuscitation followed by nimesulide treatment would save a number of patients from permanent cerebral damage.…”

Section: Discussionmentioning

confidence: 99%

“…In humans after cardiac arrest with resuscitation or cardiopulmonary bypass surgery, cerebral ischemia can lead to problems with cognition and memory, to serious neurological problems such as sensorimotor deficits and seizures, and to death (Levy et al, 1985;Petito et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

“…In humans and in animals subjected to transient forebrain ischemia, specific neurons degenerate following the ischemic episode (Kirino, 1982(Kirino, , 2000Pulsinelli et al, 1982;Petito et al, 1987). The cornu Ammonis 1 (CA1) neurons of the hippocampus are widely regarded as among the most vulnerable in the mammalian brain to ischemia (Pulsinelli et al, 1982;Kirino, 1982).…”

Section: Introductionmentioning

confidence: 99%

“…Several lines of recent evidences have shown that several pro-inflammatory genes or mediators, such as inducible nitric oxide synthase (iNOS), cyclooxygenase-2 and cytokines (e.g., tumor necrosis factor α and interleukin-1β) are strongly expressed in the ischemic brain (Ohtsuki et al, 1996;Koistinaho and Hökfelt, 1997;Barone and Feuerstein, 1999). Inflammation is now recognized as a significant contributing mechanism in cerebral ischemia because anti-inflammatory compounds or inhibitors of iNOS and cyclooxygenase-2 have been proven to reduce ischemic brain damage (Nogawa et al, 1997;Iadecola, 1997;Nakayama et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

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Neuroprotective efficacy of nimesulide against hippocampal neuronal damage following transient forebrain ischemia

Candelario‐Jalil

Alvarez

González-Falcón

et al. 2002

European Journal of Pharmacology

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Cyclooxygenase-2 is involved in the inflammatory component of the ischemic cascade, playing an important role in the delayed progression of the brain damage. The present study evaluated the pharmacological effects of the selective cyclooxygenase-2 inhibitor nimesulide on delayed neuronal death of hippocampal CA1 neurons following transient global cerebral ischemia in gerbils.Administration of therapeutically relevant doses of nimesulide (3, 6 and 12 mg/kg; i.p.) 30 minutes before ischemia and at 6, 12, 24, 48 and 72 h after ischemia significantly (P<0.01) reduced hippocampal neuronal damage. Treatment with a single dose of nimesulide given 30 min before ischemia also resulted in a significant increase in the number of healthy neurons in the hippocampal CA1 sector 7 days after ischemia. Of interest is the finding that nimesulide rescued CA1 pyramidal neurons from ischemic death even when treatment was delayed until 24 h after ischemia (34 ± 9 % protection). Neuroprotective effect of nimesulide is still evident 30 days after the ischemic episode, providing the first experimental evidence that cyclooxygenase-2 inhibitors confer a long lasting neuroprotection. Oral administration of nimesulide was also able to significantly reduce brain damage, suggesting that protective effects are independent of the route of administration. The present study confirms the ability of cyclooxygenase-2 inhibitors to reduce brain damage induced by cerebral ischemia and indicates that nimesulide can provide protection when administered for up to 24 h post-ischemia.

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CDP-choline: Neuroprotection in transient forebrain ischemia of gerbils

1999

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CDP‐choline is a rate‐limiting intermediate in the biosynthesis of phosphatidylcholine (PtdCho), an important component of the neural cell membrane. The ability of CDP‐choline to alter phospholipid metabolism is an important function in the treatment of ischemic injury. Exogenous treatment with CDP‐choline stimulates PtdCho synthesis and prevents release of free fatty acids (FFA), especially arachidonic acid (AA), after ischemia/reperfusion. Phase III clinical trials of CDP‐choline in the treatment of stroke are currently underway. Here we report the neuroprotection by CDP‐choline in transient forebrain ischemia of gerbils. CDP‐choline significantly attenuated the blood‐brain barrier (BBB) dysfunction after ischemia with 6‐hr reperfusion, and considerably reduced the increase of AA in FFA and leukotriene C4 (LTC4) synthesis at 1 day. Edema was significantly elevated after 1 and 2 days, but attained maximum at 3‐day reperfusion. CDP‐choline substantially attenuated edema at 3 days. Ischemia resulted in 80 ± 8% CA1 hippocampal neuronal death after 6‐day reperfusion, and CDP‐choline provided 65 ± 6% neuroprotection. CDP‐choline may act by increasing PtdCho synthesis via two pathways: (1) conversion of 1,2‐diacylglycerol to PtdCho, and (2) biosynthesis of S‐adenosyl‐L‐methionine, thus stabilizing the membrane and reducing AA release and metabolism to leukotriene C4. This would result in decreased toxicity due to AA, leukotrienes, oxygen radicals, lipid peroxidation, and altered glutamate uptake, thus limiting BBB dysfunction, edema and providing neuroprotection. J. Neurosci. Res. 58:697–705, 1999. © 1999 Wiley‐Liss, Inc.

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Induction of cyclooxygenase-2 mRNA in gerbil hippocampal neurons after transient forebrain ischemia

Cited by 27 publications

References 0 publications

Panax notoginseng Attenuates the Infarct Volume in Rat Ischemic Brain and the Inflammatory Response of Microglia

Panax notoginseng Attenuates the Infarct Volume in Rat Ischemic Brain and the Inflammatory Response of Microglia

Neuroprotective efficacy of nimesulide against hippocampal neuronal damage following transient forebrain ischemia

CDP-choline: Neuroprotection in transient forebrain ischemia of gerbils

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