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June 30, 2025Frontiers in PharmacologyOpen Access

Myricetin pre-treatment significantly decreased doxorubicin-elicited elevations in serum creatinine by 45% and blood urea nitrogen by 36% in rats.

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Why the study?

Doxorubicin's clinical use is limited by nephrotoxicity driven by oxidative stress and apoptosis, prompting investigation into the renoprotective potential of the natural flavonoid myricetin.

Does myricetin prevent doxorubicin-induced acute kidney injury in a rat model?

Population

Four groups with six rats in each group

Comparison

Control vs MYC vs DOX vs MYC + DOX

Design

Animal study

Follow-up

10 days

Key result

Myricetin pre-treatment significantly decreased doxorubicin-elicited elevations in serum creatinine by 45% and blood urea nitrogen by 36% in rats.

Authors

MKMuhammed KaradoğanBCBetul CicekKCKağan Tolga Cinisli

Discussion

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Member takes

Overview

May protect kidneys from doxorubicin toxicity experimentally; leaves open clinical translation pending human trials.

Structured PICO

Does myricetin prevent doxorubicin-induced acute kidney injury in a rat model?

P
Population
24 male albino Wistar rats were used to evaluate the protective effects of myricetin against doxorubicin-induced acute kidney injury over a 10-day period.
I
Intervention
Myricetin 100 mg/kg orally for 10 days, with a single intraperitoneal injection of doxorubicin 20 mg/kg on the eighth day
C
Comparator
Doxorubicin alone (oral saline for 10 days + doxorubicin 20 mg/kg i.p. on day 8), myricetin alone (100 mg/kg orally for 10 days), and vehicle control (oral and i.p. saline)
O
Outcome
Serum creatinine and blood urea nitrogen (BUN) levels, histopathological analysis of kidneys, oxidative stress markers (MDA, MPO, TOS, GSH, GPx, TAC), and apoptosis markers (Bax, Bcl-2, caspase-3, AIF)surrogate

Main Result

Effect estimate: 45% decrease

p-value: p=0.003

Myricetin demonstrates renoprotective effects against doxorubicin-induced acute kidney injury in rats through antioxidant and antiapoptotic mechanisms.

Limitations

  • Preclinical animal model might not accurately capture the complexity and diversity of human DOX-induced nephrotoxicity.
  • Need to illustrate the relationship between the regulation of ROS levels and apoptosis.
  • Further studies in clinical settings are required to validate the findings.
  • The single dose of MYC utilized may not be representative of the optimal protective dose for humans.

Cite This Study

Karadoğan et al. (2025) studied Doxorubicin-induced acute kidney injury (n=24). Myricetin vs. Doxorubicin only was evaluated on Serum creatinine levels (45% decrease, p=0.003). Myricetin pre-treatment significantly decreased doxorubicin-elicited elevations in serum creatinine by 45% and blood urea nitrogen by 36% in rats.

synapsesocial.com/papers/6a9ec239ee27e80b746f09e5https://doi.org/10.3389/fphar.2025.1601628
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Myricetin protects against doxorubicin-induced liver damage by modulating oxidative and inflammatory pathways2026
  2. 2Cardioprotective potentials of myricetin on doxorubicin-induced cardiotoxicity based on biochemical and transcriptomic analysis2024 · 9 citations
  3. 3In-silico and In-vivo Investigations Reveal Ameliorative Potential of Myricetin Against Doxorubicin-induced Myocardial Damage via Modulation of NF-κB Signaling Pathway2025
  4. 4Myricitrin Protects against Doxorubicin‐Induced Cardiotoxicity by Counteracting Oxidative Stress and Inhibiting Mitochondrial Apoptosis via ERK/P53 Pathway2016 · 53 citations
  5. 5Myricetin Prevents Doxorubicin-Induced Oxidative Stress and Mitochondrial Apoptotic Pathway in H9C2 Cardiac Cells2025