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.
Does ginkgetin prevent doxorubicin-induced heart failure and mitochondrial dysfunction in preclinical models?
Ginkgetin demonstrates cardioprotective effects against doxorubicin-induced heart failure in preclinical models by preserving mitochondrial function via the AMPK/Sirt1/NF-κB pathway.
Effect estimate: Approximately 20% absolute increase in LVEF compared to doxorubicin group
Absolute Event Rate: 60% vs 40%
p-value: p=<0.01
GK protects against DOX-induced HF by activating AMPK/Sirt1 and inhibiting NF-κB signaling, thereby mitigating OS, inflammation, apoptosis, and mitochondrial dysfunction.
Wang et al. (Fri,) conducted a other in 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.