Anti-inflammatory and neuroprotective effects of auraptene, a citrus coumarin, following cerebral global ischemia in mice

Cerebral ischemia causes delayed neuronal cell death in the hippocampus resulting in sequential cognitive impairments. Hyper-activated inflammation following ischemia is one of the etiologies for delayed neuronal cell death. In the present study, using a transient global ischemia mouse model, we sho...

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Veröffentlicht in:European journal of pharmacology 2013-01, Vol.699 (1-3), p.118-123
Hauptverfasser: Okuyama, Satoshi, Minami, Sona, Shimada, Naoko, Makihata, Nahomi, Nakajima, Mitsunari, Furukawa, Yoshiko
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Sprache:eng
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Zusammenfassung:Cerebral ischemia causes delayed neuronal cell death in the hippocampus resulting in sequential cognitive impairments. Hyper-activated inflammation following ischemia is one of the etiologies for delayed neuronal cell death. In the present study, using a transient global ischemia mouse model, we showed that auraptene (AUR), a citrus coumarin, effectively inhibited microglia activation, cyclooxygenase-2 expression by astrocytes, and neuronal cell death in the hippocampus following ischemic insults. These results suggest that AUR acts as a neuroprotective agent in the ischemic brain, which may be mediated by suppression of the inflammatory response.
ISSN:0014-2999
1879-0712
DOI:10.1016/j.ejphar.2012.11.043