The Therapeutic Effect of Curcumin in Quinolinic Acid-Induced Neurotoxicity in Rats is Associated with BDNF, ERK1/2, Nrf2, and Antioxidant Enzymes
by
Ricardo A. Santana-Martínez 1,†, Carlos A. Silva-Islas 1,†
,
Yessica Y. Fernández-Orihuela 1,
Diana Barrera-Oviedo 2,
José Pedraza-Chaverri 3,
Rogelio Hernández-Pando 4 and
Perla D. Maldonado 1,*
Ricardo A. Santana-Martínez 1,†, Carlos A. Silva-Islas 1,†,
Yessica Y. Fernández-Orihuela 1,
Diana Barrera-Oviedo 2,
José Pedraza-Chaverri 3,
Rogelio Hernández-Pando 4 and
Perla D. Maldonado 1,*
1
Laboratorio de Patología Vascular Cerebral, Instituto Nacional de Neurología y Neurocirugía, Insurgentes sur 3877, La Fama, Tlalpan CDMX 14269, Mexico
2
Departamento de Farmacología, Facultad de Medicina, Universidad Nacional Autónoma de Mexico, Av Universidad 3000, Coyoacán CDMX 04510, Mexico
3
Departamento de Biología, Facultad de Química, Universidad Nacional Autónoma de Mexico, Av Universidad 3000, Coyoacán CDMX 04510, Mexico
4
Laboratorio de Patología Experimental, Instituto Nacional de Ciencias Médicas y Nutrición, Vasco de Quiroga, Belisario Dominguez 15, Secc 16, Tlalpan CDMX 1408, Mexico
*
Author to whom correspondence should be addressed.
†
These authors contributed equally to this work.
Antioxidants 2019, 8(9), 388; https://doi.org/10.3390/antiox8090388
Received: 18 June 2019 / Revised: 24 August 2019 / Accepted: 29 August 2019 / Published: 11 September 2019
(This article belongs to the Special Issue Botanical Antioxidants and Neurological Diseases)
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.
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Keywords:
curcumin; BDNF; ERK1/2; Nrf2; glutathione; brain; quinolinic acid
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MDPI and ACS Style
Santana-Martínez, R.A.; Silva-Islas, C.A.; Fernández-Orihuela, Y.Y.; Barrera-Oviedo, D.; Pedraza-Chaverri, J.; Hernández-Pando, R.; Maldonado, P.D. The Therapeutic Effect of Curcumin in Quinolinic Acid-Induced Neurotoxicity in Rats is Associated with BDNF, ERK1/2, Nrf2, and Antioxidant Enzymes. Antioxidants 2019, 8, 388.
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