Evaluation of the neuroprotective potential of caffeic acid phenethyl ester in a cellular model of Parkinson's disease

Jul 8, 2020European journal of pharmacology

Protective effects of caffeic acid phenethyl ester in cells modeling Parkinson's disease

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Abstract

Caffeic Acid Phenethyl Ester (CAPE) significantly increased cell viability and decreased apoptotic cell death by approximately 20% after exposure to 150 μM 6-hydroxydopamine.

CAPE demonstrated neuroprotective effects in 6-hydroxydopamine-exposed SH-SY5Y cells.
Treatment with 1.25 μM CAPE improved mitochondrial membrane potential in affected cells.
CAPE reduced 6-hydroxydopamine-induced caspase activity by about ~2 fold.
The production of reactive oxygen species was inhibited by CAPE treatment.
CAPE partially restored levels of Bcl-2 and Akt while reducing Bax and cleaved caspase-9/caspase-9 levels following 6-hydroxydopamine exposure.

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Parkinson's disease (PD) is the second most prevalent neurodegenerative disease, and oxidative stress and mitochondrial dysfunction play a major role in the pathogenesis of PD. Since conventional therapeutics are not sufficient for the treatment of PD, the development of new agents with anti-oxidant potential is crucial. Caffeic Acid Phenethyl Ester (CAPE), a biologically active flavonoid of propolis, possesses several biological properties such as immunomodulatory, anti-inflammatory and anti-oxidative. In the present study, we investigated the neuroprotective effects of CAPE against 6-hydroxydopamine (6-OHDA)-induced SH-SY5Y cells. The neuroprotective effects were detected by using cell viability, Annexin V, Hoechst staining, total caspase activity, cell cycle, as well as western blotting. Besides, the anti-oxidative activity was measured by the production of reactive oxygen species and mitochondrial function was determined by measurement of mitochondrial membrane potential (ΔΨm). We found that CAPE significantly increased cell viability and decreased apoptotic cell death (~20%) after 150 μM 6-OHDA exposure following 24 h. 1.25 μM CAPE also prevented 6-OHDA-induced changes in condensed nuclear morphology. Furthermore, treatment with 1.25 μM CAPE increased mitochondrial membrane potential in 6-OHDA-exposed cells. CAPE inhibited 6-OHDA-induced caspase activity (~2 fold) and production of reactive oxygen species. In addition, 150 μM 6-OHDA-induced down-regulation of Bcl-2 and Akt levels and up-regulation of Bax and cleaved caspase-9/caspase-9 levels were partially restored by 1.25 μM CAPE treatment. These results revealed a neuroprotective potential of CAPE against 6-OHDA-induced apoptosis in an in vitro PD model and may be a potential therapeutic candidate for the prevention of neurodegeneration in Parkinson's Disease.

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Evaluation of the neuroprotective potential of caffeic acid phenethyl ester in a cellular model of Parkinson's disease

Abstract

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