Ibuprofen protects ischemia-induced neuronal injury via up-regulating interleukin-1 receptor antagonist expression

E. M. Park; B. P. Cho; B. T. Volpe; M. O. Cruz; T. H. Joh; S. Cho

doi:10.1016/j.neuroscience.2005.01.021

Ibuprofen protects ischemia-induced neuronal injury via up-regulating interleukin-1 receptor antagonist expression

E. M. Park, B. P. Cho, B. T. Volpe, M. O. Cruz, T. H. Joh, S. Cho

Department of Pharmacology

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

44 Scopus citations

Abstract

The inflammatory response accompanies and exacerbates the developing injury after cerebral ischemia. Ibuprofen, a non-steroidal anti-inflammatory drug, has been shown to attenuate injuries in animal models of various neurological diseases. In the present study, we investigated ibuprofen's neuroprotective effects in rats exposed to transient forebrain ischemia and in cultures exposed to oxygen glucose deprivation (OGD). Rats treated with ibuprofen after transient forebrain ischemia displayed long-lasting protection of CA1 hippocampal neurons. There were selective increases in interleukin-1 receptor antagonist gene and protein expression in ibuprofen-treated OGD microglia. Furthermore, treatment with ibuprofen in neuron/microglia co-cultures increased the number of surviving HC2S2 neurons against OGD whereas IL-1ra neutralizing antibody reversed the ibuprofen-induced neuroprotection. The data indicate that ibuprofen-induced IL-1ra secretion is involved in neuroprotection against ischemic conditions.

Original language	English
Pages (from-to)	625-631
Number of pages	7
Journal	Neuroscience
Volume	132
Issue number	3
DOIs	https://doi.org/10.1016/j.neuroscience.2005.01.021
State	Published - 2005

Bibliographical note

Funding Information:
Supported by AHA grant 0030225N (S.C.) and Burke Foundation.

Keywords

BV2 microglia
CA1 hippocampus
Global ischemia
Neuroprotection
Oxygen-glucose deprivation
Rat

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10.1016/j.neuroscience.2005.01.021

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title = "Ibuprofen protects ischemia-induced neuronal injury via up-regulating interleukin-1 receptor antagonist expression",

abstract = "The inflammatory response accompanies and exacerbates the developing injury after cerebral ischemia. Ibuprofen, a non-steroidal anti-inflammatory drug, has been shown to attenuate injuries in animal models of various neurological diseases. In the present study, we investigated ibuprofen's neuroprotective effects in rats exposed to transient forebrain ischemia and in cultures exposed to oxygen glucose deprivation (OGD). Rats treated with ibuprofen after transient forebrain ischemia displayed long-lasting protection of CA1 hippocampal neurons. There were selective increases in interleukin-1 receptor antagonist gene and protein expression in ibuprofen-treated OGD microglia. Furthermore, treatment with ibuprofen in neuron/microglia co-cultures increased the number of surviving HC2S2 neurons against OGD whereas IL-1ra neutralizing antibody reversed the ibuprofen-induced neuroprotection. The data indicate that ibuprofen-induced IL-1ra secretion is involved in neuroprotection against ischemic conditions.",

keywords = "BV2 microglia, CA1 hippocampus, Global ischemia, Neuroprotection, Oxygen-glucose deprivation, Rat",

author = "Park, {E. M.} and Cho, {B. P.} and Volpe, {B. T.} and Cruz, {M. O.} and Joh, {T. H.} and S. Cho",

note = "Funding Information: Supported by AHA grant 0030225N (S.C.) and Burke Foundation.",

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AU - Park, E. M.

AU - Cho, B. P.

AU - Volpe, B. T.

AU - Cruz, M. O.

AU - Joh, T. H.

AU - Cho, S.

N1 - Funding Information: Supported by AHA grant 0030225N (S.C.) and Burke Foundation.

PY - 2005

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N2 - The inflammatory response accompanies and exacerbates the developing injury after cerebral ischemia. Ibuprofen, a non-steroidal anti-inflammatory drug, has been shown to attenuate injuries in animal models of various neurological diseases. In the present study, we investigated ibuprofen's neuroprotective effects in rats exposed to transient forebrain ischemia and in cultures exposed to oxygen glucose deprivation (OGD). Rats treated with ibuprofen after transient forebrain ischemia displayed long-lasting protection of CA1 hippocampal neurons. There were selective increases in interleukin-1 receptor antagonist gene and protein expression in ibuprofen-treated OGD microglia. Furthermore, treatment with ibuprofen in neuron/microglia co-cultures increased the number of surviving HC2S2 neurons against OGD whereas IL-1ra neutralizing antibody reversed the ibuprofen-induced neuroprotection. The data indicate that ibuprofen-induced IL-1ra secretion is involved in neuroprotection against ischemic conditions.

AB - The inflammatory response accompanies and exacerbates the developing injury after cerebral ischemia. Ibuprofen, a non-steroidal anti-inflammatory drug, has been shown to attenuate injuries in animal models of various neurological diseases. In the present study, we investigated ibuprofen's neuroprotective effects in rats exposed to transient forebrain ischemia and in cultures exposed to oxygen glucose deprivation (OGD). Rats treated with ibuprofen after transient forebrain ischemia displayed long-lasting protection of CA1 hippocampal neurons. There were selective increases in interleukin-1 receptor antagonist gene and protein expression in ibuprofen-treated OGD microglia. Furthermore, treatment with ibuprofen in neuron/microglia co-cultures increased the number of surviving HC2S2 neurons against OGD whereas IL-1ra neutralizing antibody reversed the ibuprofen-induced neuroprotection. The data indicate that ibuprofen-induced IL-1ra secretion is involved in neuroprotection against ischemic conditions.

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KW - Global ischemia

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Ibuprofen protects ischemia-induced neuronal injury via up-regulating interleukin-1 receptor antagonist expression

Abstract

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Keywords

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