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

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 (P < 0.05) the circling MPP(+)-induced behavior (10 μg/8 μL). Likewise, EC significantly (P < 0.05) reduced the formation of fluorescent lipid products caused by MPP(+). MPP(+) injection produced (P < 0.05) 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 (P < 0.05) 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.

journal_name

Oxid Med Cell Longev

authors

Rubio-Osornio M,Gorostieta-Salas E,Montes S,Pérez-Severiano F,Rubio C,Gómez C,Ríos C,Guevara J

doi

10.1155/2015/276039

subject

Has Abstract

pub_date

2015-01-01 00:00:00

pages

276039

eissn

1942-0900

issn

1942-0994

journal_volume

2015

pub_type

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