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Brain Advance Access originally published online on October 6, 2004
Brain 2004 127(12):2629-2635; doi:10.1093/brain/awh316
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Brain Vol. 127 No. 12 © Guarantors of Brain 2004; all rights reserved

Caffeic acid phenethyl ester prevents neonatal hypoxic–ischaemic brain injury

Xing Wei1,*, Liming Zhao1,*, Zhizhong Ma1, David M. Holtzman2, Chong Yan1, Richard C. Dodel3, Harald Hampel4, Wolfgang Oertel5, Martin R. Farlow1 and Yansheng Du1,*

1 Department of Neurology, School of Medicine, Indiana University, Indianapolis, IN, 2 Department of Neurology, Molecular Biology and Pharmacology, Washington University School of Medicine, St Louis, MO, USA, 3 Department of Neurology, Friedrich-Wilhelms University, Bonn, 4 Department of Psychiatry, Ludwig-Maximilian University, Munich and 5 Department of Neurology, Philipps University, Marburg, Germany

Correspondence to: Yansheng Du, PhD, Department of Neurology, Indiana University School of Medicine, 975 W. Walnut Street IB 457, Indianapolis, IN 46202, USA E-mail: ydu{at}iupui.edu

Neonatal hypoxic–ischaemic (HI) brain injury resulting in encephalopathy is a leading cause of morbidity and mortality with no effective treatment. Here we show that caffeic acid phenethyl ester (CAPE), an active component of propolis, administered either before or after an HI insult, significantly prevents HI-induced neonatal rat brain damage in the cortex, hippocampus and thalamus. In addition to blocking HI-induced caspase 3 activation, CAPE also inhibits HI-mediated expression of inducible nitric oxide synthase and caspase 1 in vivo and potently blocks nitric oxide-induced neurotoxicity in vitro. Furthermore, CAPE directly inhibits Ca2+-induced cytochrome c release from isolated brain mitochondria. Thus, CAPE induces neuroprotection against HI-induced neuronal death, possibly by blocking HI-induced inflammation and/or directly inhibiting the HI-induced neuronal death pathway. CAPE may therefore be a novel effective therapy for preventing neonatal HI injury.


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