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. 2021 Aug 30:2021:5553480.
doi: 10.1155/2021/5553480. eCollection 2021.

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

Affiliations

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

Burak Cem Soner et al. Parkinsons Dis. .

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.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Figure 1
Figure 1
The experimental schedule.
Figure 2
Figure 2
The ratio of contralateral lesion side (left side) tape playing time versus total playing time. Adhesive tape removal test results of control, CAPE 20, and CAPE 80 groups before (termed as pretest) and after (termed as posttest) 6-OHDA application. Control group, n = 7; CAPE 20 group, n = 9; CAPE 80 group, n = 8. p < 0.01 versus control posttest.
Figure 3
Figure 3
The numbers show the activity level as the total number of squares crossed during a 5 min testing period. Intrastriatal CAPE treatment (20 and 80 μmol/5 μL) reversed the decreases in locomotor activity observed in the 6-OHDA-lesioned group, and this protective effect was higher in the CAPE 80 group. Control group, n = 7; CAPE 20 group, n = 9; CAPE 80 group, n = 8 (p < 0.01 versus control posttest, ∗∗p < 0.05 versus control posttest; #p < 0.05 versus CAPE 20 posttest).
Figure 4
Figure 4
Data were presented as the left forepaw contacts as a percentage of the total number of contacts of each forepaw. Preferences in the forelimb usage of groups are given. Control group, n = 7; CAPE 20 group, n = 9; CAPE 80 group, n = 8 (p < 0.01 versus control-pretest; #p < 0.05 versus CAPE 20-pretest; and ∗∗p < 0.01 versus control posttest).
Figure 5
Figure 5
0.25 mg/kg apomorphine-induced contralateral rotations in 40 min for control (6-OHDA-induced lesion rats), CAPE 20, and CAPE 80 groups. Control group, n = 7; CAPE 20 group, n = 9; CAPE 80 group, n = 8. ∗∗p < 0.01 versus control.
Figure 6
Figure 6
(a) Control group (6-OHDA-induced lesion rats); (b) CAPE 20 group; (c) CAPE 80 group. cc: corpus callusum, Cx : cortex, Str: striatum. Magnification ×400. Internal scale bar = 500 μm.
Figure 7
Figure 7
TH-immunostained striatal fiber density (OD) quantified using ImageJ. Control group, n = 7; CAPE 20 group, n = 9; CAPE 80 group, n = 8. p < 0.05 CAPE-20 vs. control; and #p < 0.01 vs. CAPE-80 vs control.

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