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Brain Advance Access published online on October 6, 2004
Brain, doi:10.1093/brain/awh316
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Received June 9, 2004
Revised August 31, 2004
Accepted September 8, 2004

Article

Caffeic acid phenethyl ester prevents neonatal hypoxic-ischaemic brain injury

Xing Wei 1, Liming Zhao 1, Zhizhong Ma 1, David M. Holtzman 2, Chong Yan 1, Richard C. Dodel 3, Harald Hampel 4, Wolfgang Oertel 5, Martin R. Farlow 1, and Yansheng Du 1*

1 Department of Neurology, School of Medicine, Indiana University, Indianapolis, IN, USA
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, Germany
4 Department of Psychiatry, Ludwig-Maximilian University, Munich, Germany
5 Department of Neurology, Philipps University, Marburg, Germany

* To whom correspondence should be addressed. E-mail: ydu{at}iupui.edu.


  Abstract

Summary 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.

Keywords: brain injury; hypoxia-ischaemia; caffeic acid phenethyl ester; rat.
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