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Candesartan protects from cisplatin-induced kidney damage via the GDF-15 pathway

G Güner1, O Erbaş

  • 1Department of Medical Oncology, Medical Point Hospital, University of Economy, Izmir, Turkey. gurkan.guner@izmirekonomi.edu.tr.

European Review for Medical and Pharmacological Sciences
|February 20, 2024
PubMed
Abstract

Insights

Candesartan protects against cisplatin-induced kidney damage by increasing growth differentiation factor 15 (GDF-15) and reducing inflammation and oxidative stress.

Area of Science:

  • Nephrology
  • Pharmacology
  • Toxicology

Background:

  • Cisplatin is a widely used chemotherapy agent with significant nephrotoxic side effects.
  • Identifying strategies to mitigate cisplatin-induced kidney damage is crucial for improving patient outcomes.
  • The role of growth differentiation factor 15 (GDF-15) in renal protection warrants further investigation.

Purpose of the Study:

  • To investigate the protective effects of candesartan on cisplatin-induced nephrotoxicity.
  • To explore the involvement of the GDF-15 pathway in candesartan's renoprotective mechanism.

Main Methods:

  • Adult female Wistar rats were administered cisplatin to induce kidney damage.
  • Animals were treated with either candesartan or a placebo (tap water).
  • Kidney histology, serum creatinine, malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and GDF-15 levels were assessed.

Main Results:

  • Candesartan treatment significantly reduced serum levels of MDA, TNF-α, IL-6, and creatinine compared to the cisplatin-only group.
  • Serum GDF-15 levels were significantly elevated in rats treated with candesartan.
  • Histopathological examination confirmed that candesartan protected against kidney injury.

Conclusions:

  • Candesartan demonstrates significant renoprotective effects against cisplatin-induced nephrotoxicity.
  • The mechanism involves increasing GDF-15 levels, downregulating inflammatory markers, and reducing oxidative stress.
  • Candesartan represents a potential therapeutic strategy to mitigate chemotherapy-related kidney damage.

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