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February 8, 20260 citations

Ginkgetin Alleviates Doxorubicin-Induced Heart Failure by Regulating Mitochondrial Dysfunction Through the AMPK/Sirt1/NF-κB Signaling Pathway.

YWYanfu WangHLHang LiuWLWei Li

Key Result

Ginkgetin at 100 mg/kg dose increased left ventricular ejection fraction by approximately 20% compared to doxorubicin alone in mice with doxorubicin-induced heart failure.

Key Points

  • The study aims to evaluate the protective effects of ginkgetin on doxorubicin-induced heart failure by targeting mitochondrial dysfunction.
  • Utilized an experimental model of heart failure induced by doxorubicin.
  • Administered ginkgetin to assess its effects on heart function.
  • Analyzed the expression of AMPK, Sirt1, and NF-κB signaling pathways.
  • Evaluated oxidative stress, inflammation, and apoptosis indicators.
  • Ginkgetin treatment significantly activated AMPK and Sirt1 pathways.
  • Reduction in NF-κB activity was observed, leading to decreased inflammation.
  • Marked improvement in mitochondrial function was noted, mitigating oxidative stress and apoptosis.

Structured PICO

Does ginkgetin prevent doxorubicin-induced heart failure and mitochondrial dysfunction in preclinical models?

P
Population
Male C57BL/6 mice (8 weeks old, 20–25 g, n=36) and H9c2 rat cardiomyocyte line.
I
Intervention
Ginkgetin (25, 50, or 100 mg/kg once weekly for six weeks) in mice; Ginkgetin (5, 10, or 20 μM for 24 hours) in H9c2 cells.
C
Comparator
Doxorubicin (5 mg/kg once weekly for four weeks) alone, and normal saline control.
O
Outcome
Cardiac function (LVEF, LVFS, LVIDs, LVIDd, E/A ratio), myocardial injury markers, oxidative stress, inflammation, apoptosis, and mitochondrial function.surrogate

Ginkgetin demonstrates cardioprotective effects against doxorubicin-induced heart failure in preclinical models by preserving mitochondrial function via the AMPK/Sirt1/NF-κB pathway.

Main Result

Effect estimate: Approximately 20% absolute increase in LVEF compared to doxorubicin group

Absolute Event Rate: 60% vs 40%

p-value: p=<0.01

Limitations

  • Study conducted only in male mice; results may not generalize to females or humans.
  • Small sample size (n=6 per group) limiting statistical power.
  • Animal and cellular models, no clinical trial data available.
  • Lack of long-term follow-up data post-treatment.
  • No a priori sample size calculation was performed

Abstract

GK protects against DOX-induced HF by activating AMPK/Sirt1 and inhibiting NF-κB signaling, thereby mitigating OS, inflammation, apoptosis, and mitochondrial dysfunction.

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Cite This Study

Wang et al. (2026) studied Male C57BL/6 mice aged 8 weeks with doxorubicin-induced heart failure (n=30). Ginkgetin vs. Control (normal saline) and doxorubicin only groups was evaluated on Cardiac function measured by left ventricular ejection fraction (LVEF) (Approximately 20% absolute increase in LVEF compared to doxorubicin group, p=<0.01). Ginkgetin at 100 mg/kg dose increased left ventricular ejection fraction by approximately 20% compared to doxorubicin alone in mice with doxorubicin-induced heart failure.

synapsesocial.com/papers/698828620fc35cd7a8847ca9https://doi.org/10.4274/balkanmedj.galenos.2026.2025-11-113
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