Neuroprotective effect of caffeic acid phenethyl ester in 3-nitropropionic acid-induced striatal neurotoxicity.
10.4196/kjpp.2016.20.3.279
- Author:
Jia BAK
1
;
Hee Jung KIM
;
Seong Yun KIM
;
Yun Sik CHOI
Author Information
1. Department of Pharmaceutical Science and Technology, College of Health and Medical Science, Catholic University of Daegu, Gyeongsan 38430, Korea. tiana@cu.ac.kr
- Publication Type:Original Article
- Keywords:
3-nitropropionic acid;
Antioxidant;
Caff eic acid phenethyl ester;
Huntington's disease;
Striatum
- MeSH:
Animals;
Astrocytes;
Body Weight;
Cell Death;
Dimethyl Sulfoxide;
Glial Fibrillary Acidic Protein;
Humans;
Huntington Disease;
Male;
Mice;
Microglia;
Models, Chemical;
Mortality;
Neurons;
Neuroprotective Agents*;
Rotarod Performance Test;
Urticaria
- From:The Korean Journal of Physiology and Pharmacology
2016;20(3):279-286
- CountryRepublic of Korea
- Language:English
-
Abstract:
Caffeic acid phenethyl ester (CAPE), derived from honeybee hives, is a bioactive compound with strong antioxidant activity. This study was designed to test the neuroprotective effect of CAPE in 3-nitropropionic acid (3NP)-induced striatal neurotoxicity, a chemical model of Huntington's disease (HD). Initially, to test CAPE's antioxidant activity, a 2,2'-azino-bis-3-ethylbenzthiazoline-6-sulfonic acid (ABTS) antioxidant assay was employed, and CAPE showed a strong direct radical-scavenging eff ect. In addition, CAPE provided protection from 3NP-induced neuronal cell death in cultured striatal neurons. Based on these observations, the in vivo therapeutic potential of CAPE in 3NP-induced HD was tested. For this purpose, male C57BL/6 mice were repeatedly given 3NP to induce HD-like pathogenesis, and 30 mg/kg of CAPE or vehicle (5% dimethyl sulfoxide and 95% peanut oil) was administered daily. CAPE did not cause changes in body weight, but it reduced mortality by 29%. In addition, compared to the vehicle-treated group, robustly reduced striatal damage was observed in the CAPE-treated animals, and the 3NP-induced behavioral defi cits on the rotarod test were signifi cantly rescued after the CAPE treatment. Furthermore, immunohistochemical data showed that immunoreactivity to glial fibrillary acidic protein (GFAP) and CD45, markers for astrocyte and microglia activation, respectively, were strikingly reduced. Combined, these data unequivocally indicate that CAPE has a strong antioxidant eff ect and can be used as a potential therapeutic agent against HD.
