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Negrette-Guzmán M, García-Niño WR, Tapia E, et al. Curcumin Attenuates Gentamicin-Induced Kidney Mitochondrial Alterations: Possible Role of a Mitochondrial Biogenesis Mechanism. Evid Based Complement Alternat Med. 2015;2015:917435doi: 10.1155/2015/917435.
Negrette-Guzmán, M., García-Niño, W. R., Tapia, E., Zazueta, C., Huerta-Yepez, S., León-Contreras, J. C., Hernández-Pando, R., Aparicio-Trejo, O. E., Madero, M., & Pedraza-Chaverri, J. (2015). Curcumin Attenuates Gentamicin-Induced Kidney Mitochondrial Alterations: Possible Role of a Mitochondrial Biogenesis Mechanism. Evidence-based complementary and alternative medicine : eCAM, 2015917435. https://doi.org/10.1155/2015/917435
Negrette-Guzmán, Mario, et al. "Curcumin Attenuates Gentamicin-Induced Kidney Mitochondrial Alterations: Possible Role of a Mitochondrial Biogenesis Mechanism." Evidence-based complementary and alternative medicine : eCAM vol. 2015 (2015): 917435. doi: https://doi.org/10.1155/2015/917435
Negrette-Guzmán M, García-Niño WR, Tapia E, Zazueta C, Huerta-Yepez S, León-Contreras JC, Hernández-Pando R, Aparicio-Trejo OE, Madero M, Pedraza-Chaverri J. Curcumin Attenuates Gentamicin-Induced Kidney Mitochondrial Alterations: Possible Role of a Mitochondrial Biogenesis Mechanism. Evid Based Complement Alternat Med. 2015;2015:917435. doi: 10.1155/2015/917435. Epub 2015 Aug 05. PMID: 26345660; PMCID: PMC4541007.
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Evid Based Complement Alternat Med. 2015;2015:917435. doi: 10.1155/2015/917435. Epub 2015 Aug 05.

Curcumin Attenuates Gentamicin-Induced Kidney Mitochondrial Alterations: Possible Role of a Mitochondrial Biogenesis Mechanism.

Evidence-based complementary and alternative medicine : eCAM

Mario Negrette-Guzmán, Wylly Ramsés García-Niño, Edilia Tapia, Cecilia Zazueta, Sara Huerta-Yepez, Juan Carlos León-Contreras, Rogelio Hernández-Pando, Omar Emiliano Aparicio-Trejo, Magdalena Madero, José Pedraza-Chaverri

Affiliations

  1. Departamento de Biología, Facultad de Química, UNAM, 04510 Ciudad de México, DF, Mexico.
  2. Departamento de Biomedicina Cardiovascular, Instituto Nacional de Cardiología "Ignacio Chávez", 14080 Ciudad de México, DF, Mexico.
  3. Laboratorio de Fisiopatología Renal, Instituto Nacional de Cardiología "Ignacio Chávez", 14080 Ciudad de México, DF, Mexico.
  4. Unidad de Investigación en Enfermedades Oncológicas, Hospital Infantil de México "Federico Gómez", 06720 Ciudad de México, DF, Mexico.
  5. Departamento de Patología, Instituto Nacional de Ciencias Médicas y Nutrición "Salvador Zubirán", 14000 Ciudad de México, DF, Mexico.
  6. Departamento de Nefrología, Instituto Nacional de Cardiología "Ignacio Chávez", 14080 Ciudad de México, DF, Mexico.

PMID: 26345660 PMCID: PMC4541007 DOI: 10.1155/2015/917435

Abstract

It has been shown that curcumin (CUR), a polyphenol derived from Curcuma longa, exerts a protective effect against gentamicin- (GM-) induced nephrotoxicity in rats, associated with a preservation of the antioxidant status. Although mitochondrial dysfunction is a hallmark in the GM-induced renal injury, the role of CUR in mitochondrial protection has not been studied. In this work, LLC-PK1 cells were preincubated 24 h with CUR and then coincubated 48 h with CUR and 8 mM GM. Treatment with CUR attenuated GM-induced drop in cell viability and led to an increase in nuclear factor (erythroid-2)-related factor 2 (Nrf2) nuclear accumulation and peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) cell expression attenuating GM-induced losses in these proteins. In vivo, Wistar rats were injected subcutaneously with GM (75 mg/Kg/12 h) during 7 days to develop kidney mitochondrial alterations. CUR (400 mg/Kg/day) was administered orally 5 days before and during the GM exposure. The GM-induced mitochondrial alterations in ultrastructure and bioenergetics as well as decrease in activities of respiratory complexes I and IV and induction of calcium-dependent permeability transition were mostly attenuated by CUR. Protection of CUR against GM-induced nephrotoxicity could be in part mediated by maintenance of mitochondrial functions and biogenesis with some participation of the nuclear factor Nrf2.

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