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Oxidative Medicine and Cellular Longevity
Volume 2015, Article ID 276039, 6 pages
http://dx.doi.org/10.1155/2015/276039
Research Article

Epicatechin Reduces Striatal MPP+-Induced Damage in Rats through Slight Increases in SOD-Cu,Zn Activity

1Laboratorio Experimental de Enfermedades Neurodegenerativas, Instituto Nacional de Neurología y Neurocirugía, Manuel Velasco Suárez, 14269 Mexico City, Mexico
2Departamento de Neuroquímica, Instituto Nacional de Neurología y Neurocirugía, Manuel Velasco Suárez, 14269 Mexico City, Mexico
3Departamento de Farmacología, Facultad de Medicina, Universidad Nacional Autónoma de México, 04510 Mexico City, Mexico
4Departamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, 04510 Mexico City, Mexico

Received 6 February 2015; Revised 2 May 2015; Accepted 11 May 2015

Academic Editor: Sathyasaikumar V. Korrapati

Copyright © 2015 M. Rubio-Osornio et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Parkinson’s disease is a neurodegenerative disorder characterized by movement alterations caused by reduced dopaminergic neurotransmission in the nigrostriatal pathway, presumably by oxidative stress (OS). MPP+ intrastriatal injection leads to the overproduction of free radicals (FR). The increasing formation of FR produces OS, a decline in dopamine (DA) content, and behavioral disorders. Epicatechin (EC) has shown the ability to be FR scavenger, an antioxidant enzyme inductor, a redox state modulator, and transition metal chelator. Acute administration of 100 mg/kg of EC significantly prevented () the circling MPP+-induced behavior (10 μg/8 μL). Likewise, EC significantly () reduced the formation of fluorescent lipid products caused by MPP+. MPP+ injection produced () increased enzymatic activity of the constitutive nitric oxide synthase (cNOS). This effect was blocked with acute EC pretreatment. Cu/Zn-dependent superoxide dismutase (Cu/Zn-SOD) activity was significantly () reduced as a consequence of MPP+ damage. EC produced a slight increase (≈20%) in Cu/Zn-SOD activity in the control group. Such effects persisted in animals injured with MPP+. The results show that EC is effective against MPP+-induced biochemical and behavioral damage, which is possible by an increase in Cu/Zn-SOD activity.