| Autor: |
Santana-Martínez RA; Laboratorio de Patología Vascular Cerebral, Instituto Nacional de Neurología y Neurocirugía, Insurgentes sur 3877, La Fama, Tlalpan CDMX 14269, Mexico. ricartiani@hotmail.com., Silva-Islas CA; Laboratorio de Patología Vascular Cerebral, Instituto Nacional de Neurología y Neurocirugía, Insurgentes sur 3877, La Fama, Tlalpan CDMX 14269, Mexico., Fernández-Orihuela YY; Laboratorio de Patología Vascular Cerebral, Instituto Nacional de Neurología y Neurocirugía, Insurgentes sur 3877, La Fama, Tlalpan CDMX 14269, Mexico. yessicayaelfdz@gmail.com., Barrera-Oviedo D; Departamento de Farmacología, Facultad de Medicina, Universidad Nacional Autónoma de Mexico, Av Universidad 3000, Coyoacán CDMX 04510, Mexico. dianabarrera@hotmail.com., Pedraza-Chaverri J; Departamento de Biología, Facultad de Química, Universidad Nacional Autónoma de Mexico, Av Universidad 3000, Coyoacán CDMX 04510, Mexico. pedraza@unam.mx., Hernández-Pando R; Laboratorio de Patología Experimental, Instituto Nacional de Ciencias Médicas y Nutrición, Vasco de Quiroga, Belisario Dominguez 15, Secc 16, Tlalpan CDMX 1408, Mexico. rhdezpando@hotmail.com., Maldonado PD; Laboratorio de Patología Vascular Cerebral, Instituto Nacional de Neurología y Neurocirugía, Insurgentes sur 3877, La Fama, Tlalpan CDMX 14269, Mexico. maldonado.perla@gmail.com. |
| Abstrakt: |
In the present study we investigated the participation of brain-derived neurotropic factor (BDNF) on the activation of the mitogen activated protein kinase (MAPK) protein extracellular signal-regulated kinase-1/2 (ERK1/2) as a mechanism of curcumin (CUR) to provide an antioxidant defense system mediated by the nuclear factor erythroid 2-related factor 2 (Nrf2) in the neurotoxic model induced by quinolinic acid (QUIN). Wistar rats received CUR (400 mg/kg, intragastrically) for 6 days after intrastriatal injection with QUIN (240 nmol). CUR improved the motor deficit and morphological alterations induced by QUIN and restored BDNF, ERK1/2, and Nrf2 levels. CUR treatment avoided the decrease in the protein levels of glutathione peroxidase (GPx), glutathione reductase (GR), γ-glutamylcysteine ligase (γ-GCL), and glutathione (GSH) levels. Only, the QUIN-induced decrease in the GR activity was prevented by CUR treatment. Finally, QUIN increased superoxide dismutase 2 (SOD2) and catalase (CAT) levels, and the γGCL and CAT activities; however, this increase was major in the QUIN+CUR group for γ-GCL, CAT, and SOD activities. These data suggest that the therapeutic effect of CUR could involve BDNF action on the activation of ERK1/2 to induce increased levels of protein and enzyme activity of antioxidant proteins regulated by Nrf2 and GSH levels. |
