Neuroprotective Effect of Intrastriatal Caffeic Acid Phenethyl Ester Treatment in 6-OH Dopamine Model of Parkinson's Disease in Rats.

Burak Cem Soner,Salim Yalcin Inan,Ayse Saide Sahin,Eda Acikgoz,Gulperi Oktem,Sule Ayla,Cristine Alves Da Costa

doi:10.1155/2021/5553480

Abstract

Parkinson's disease (PD) is the second most common neurodegenerative disorder, and the main cause of PD is still not known. Until now, no cure for Parkinson's disease is yet in sight. Caffeic acid phenethyl ester (CAPE) is a polyphenolic component of the propolis, which can be derived from honeybee hive propolis. We aimed to determine the effect of intrastriatal CAPE administration as a neuroprotective agent on 6-hydroxydopamine (6-OHDA)-induced PD model. Adult male Wistar rats weighing 280–320 g were used. The PD model was induced with unilateral intrastriatal 6-OHDA injection. Treatment groups received 20 μmol/5 μL/4 day and 80 μmol/5 μL/4 day CAPE 24 h after 6-OHDA injection. Eight days after 6-OHDA application, behavioral studies (adhesive tape removal test, open-field test, cylinder test, and apomorphine-induced asymmetric rotational behavior) were performed once more to compare the effects of CAPE on behavior tests. Striatal histological verifications, immunohistochemistry, and stereological quantitation were performed. Our results for the first time showed that, besides improving the motor performance, CAPE treatment also prevents 6-OHDA-induced loss of TH-positive neurons. From our results, CAPE may be a promising clinical agent in the treatment of PD.

Highlights

Parkinson’s disease (PD) is defined as the second most common neurodegenerative disorder after Alzheimer’s disease and is characterized by the progressive loss of dopaminergic neurons in substantia nigra pars compacta. e main cause of PD is still not known
Besides improving the motor performance, Caffeic acid phenethyl ester (CAPE) treatment inhibits 6-OHDA
CAPE treatment prevents 6-OHDAinduced loss of tyrosine hydroxylase (TH)-positive neurons. ese results for the first time established the intrastriatal protective dose of CAPE and its in vivo protecting effect on behavioral tests against 6-OHDA mediated PD model in rats

Summary

Introduction

Parkinson’s disease (PD) is defined as the second most common neurodegenerative disorder after Alzheimer’s disease and is characterized by the progressive loss of dopaminergic neurons in substantia nigra pars compacta. e main cause of PD is still not known. Parkinson’s disease (PD) is defined as the second most common neurodegenerative disorder after Alzheimer’s disease and is characterized by the progressive loss of dopaminergic neurons in substantia nigra pars compacta. Clinical signs of the disease appear after a 60–65% dopaminergic neuronal loss at substantia nigra, and a 80–85% dopamine level decrease at striatum [4]. 50% slowing down in the progression of the disease will have a 35% decrease in the economic implications and minimize the negative impact of the symptoms [5]. Treatment modalities are mostly based on reducing the symptoms and/or stimulation of neurodegenerated dopaminergic neurons, [6] and, current research strategies and treatment approaches are Parkinson’s Disease headed towards the prevention of dopaminergic neuronal loss [7]

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