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The flavanoide caffeic acid phenethyl ester blocks 6-hydroxydopamine-induced neurotoxicity.
Neurosci Lett. 2005 Jul 22-29; 383(1-2):39-43.NL

Abstract

Parkinson's disease (PD) is a neurodegenerative disorder characterized by progressive loss of dopaminergic (DA) neurons of the substantia nigra pars compacta. 6-Hydroxydopamine (6-OHDA) is specific to dopaminergic neurons in intrastriatal rodent models. It induces neuronal death either via uncoupling mitochondrial oxidative phosphorylation resulting in energy deprivation or alternatively, is associated with its ability to produce hydrogen peroxide, hydroxyl and superoxide radicals. Caffeic acid phenethyl ester (CAPE), an antioxidant flavanoid, has antiviral, anti-inflammatory, antioxidant, and immunomodulatory properties. Recent studies have shown that CAPE has also a neuroprotective effects in ischemia and low potassium-induced neuronal apoptotic models. In cerebellar granule neurons CAPE significantly blocks 6-OHDA mediated cell death (70 microM) in a dose-dependent manner. Furthermore, CAPE was able to modulate the Ca(2+)-induced release of cyctochrome c in isolated liver mitochondria. Caspase-3 activation following 6-OHDA treatment was markedly inhibited in the presence of CAPE. Although the molecular mechanisms associated with CAPE's neuroprotective effects remain to be elucidated in more detail, our results clearly demonstrate a considerable neuroprotective effect of CAPE. Since a mitochondrial insult is a major cause for the degeneration of nigral neurons in PD, we hypothesize that propolis derivatives, in particular CAPE, may have a neuroprotective effect on those cells and may be a promising drug candidate to be taken into in vivo models of PD.

Authors+Show Affiliations

Department of Neurology, Friedrich-Wilhelms-University, Bonn, Germany.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

15894425

Citation

Noelker, Carmen, et al. "The Flavanoide Caffeic Acid Phenethyl Ester Blocks 6-hydroxydopamine-induced Neurotoxicity." Neuroscience Letters, vol. 383, no. 1-2, 2005, pp. 39-43.
Noelker C, Bacher M, Gocke P, et al. The flavanoide caffeic acid phenethyl ester blocks 6-hydroxydopamine-induced neurotoxicity. Neurosci Lett. 2005;383(1-2):39-43.
Noelker, C., Bacher, M., Gocke, P., Wei, X., Klockgether, T., Du, Y., & Dodel, R. (2005). The flavanoide caffeic acid phenethyl ester blocks 6-hydroxydopamine-induced neurotoxicity. Neuroscience Letters, 383(1-2), 39-43.
Noelker C, et al. The Flavanoide Caffeic Acid Phenethyl Ester Blocks 6-hydroxydopamine-induced Neurotoxicity. Neurosci Lett. 2005 Jul 22-29;383(1-2):39-43. PubMed PMID: 15894425.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The flavanoide caffeic acid phenethyl ester blocks 6-hydroxydopamine-induced neurotoxicity. AU - Noelker,Carmen, AU - Bacher,Michael, AU - Gocke,Petra, AU - Wei,Xing, AU - Klockgether,Thomas, AU - Du,Yansheng, AU - Dodel,Richard, PY - 2005/02/18/received PY - 2005/04/01/revised PY - 2005/04/02/accepted PY - 2005/5/17/pubmed PY - 2005/8/23/medline PY - 2005/5/17/entrez SP - 39 EP - 43 JF - Neuroscience letters JO - Neurosci Lett VL - 383 IS - 1-2 N2 - Parkinson's disease (PD) is a neurodegenerative disorder characterized by progressive loss of dopaminergic (DA) neurons of the substantia nigra pars compacta. 6-Hydroxydopamine (6-OHDA) is specific to dopaminergic neurons in intrastriatal rodent models. It induces neuronal death either via uncoupling mitochondrial oxidative phosphorylation resulting in energy deprivation or alternatively, is associated with its ability to produce hydrogen peroxide, hydroxyl and superoxide radicals. Caffeic acid phenethyl ester (CAPE), an antioxidant flavanoid, has antiviral, anti-inflammatory, antioxidant, and immunomodulatory properties. Recent studies have shown that CAPE has also a neuroprotective effects in ischemia and low potassium-induced neuronal apoptotic models. In cerebellar granule neurons CAPE significantly blocks 6-OHDA mediated cell death (70 microM) in a dose-dependent manner. Furthermore, CAPE was able to modulate the Ca(2+)-induced release of cyctochrome c in isolated liver mitochondria. Caspase-3 activation following 6-OHDA treatment was markedly inhibited in the presence of CAPE. Although the molecular mechanisms associated with CAPE's neuroprotective effects remain to be elucidated in more detail, our results clearly demonstrate a considerable neuroprotective effect of CAPE. Since a mitochondrial insult is a major cause for the degeneration of nigral neurons in PD, we hypothesize that propolis derivatives, in particular CAPE, may have a neuroprotective effect on those cells and may be a promising drug candidate to be taken into in vivo models of PD. SN - 0304-3940 UR - https://www.unboundmedicine.com/medline/citation/15894425/The_flavanoide_caffeic_acid_phenethyl_ester_blocks_6_hydroxydopamine_induced_neurotoxicity_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304-3940(05)00396-4 DB - PRIME DP - Unbound Medicine ER -