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Gliclazide attenuates cisplatin-induced nephrotoxicity through inhibiting NF-κB and caspase-3 activity.

F. Taghizadeh,S. Hosseinimehr,M. Zargari,A. Karimpour Malekshah,Fereshteh Beigom Talebpour Amiri

Published 2020 in IUBMB Life - A Journal of the International Union of Biochemistry and Molecular Biology

ABSTRACT

Cisplatin (CP), as a chemotherapeutic drug, causes nephrotoxicity that has limited the clinical utility of CP. Gliclazide (GLZ), as an antihyperglycemic drug, at low dose has antioxidant property. In this study, we aimed to investigate the protective effect of GLZ against CP-induced acute renal injury. Sixty-four BALB/c mice were randomly divided into eight groups. The groups were included as control, GLZ (5, 10, and 25 mg/kg), CP, and GLZ (5, 10, and 25 mg/kg) + CP. Renal function markers (serum creatinine and blood urea nitrogen), oxidative stress markers (malondialdehyde and glutathione), apoptotic marker (caspase-3), and NF-κB were histopathologically evaluated. The results of our study showed that increased urea and creatinine were evidence of CP-induced nephrotoxicity. Histopathological examination revealed tubular epithelial and Bowman degeneration, edema, and cytoplasmic vacuolation in renal tissue structure. Administration of GLZ reduced oxidative stress, caspase-3, and NF-κB activity, and improved kidney function markers in CP-treated mice compared with CP alone group. Also, we observed that the histological tissue structure of the kidney was maintained. GLZ at dose of 25 mg/kg had higher protective effect as compared with other doses. Overall, our study suggests that GLZ with antioxidant, antiapoptotic, and anti-inflammatory properties may be a promising new therapeutic agent to prevent CP-induced nephrotoxicity.

PUBLICATION RECORD

  • Publication year

    2020

  • Venue

    IUBMB Life - A Journal of the International Union of Biochemistry and Molecular Biology

  • Publication date

    2020-07-20

  • Fields of study

    Medicine

  • Identifiers
    DOI 10.1002/iub.2342PMID 32687680
  • External record

    Open on Semantic Scholar

  • Source metadata

    Semantic Scholar, PubMed

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