Key result
Vinpocetine protected against doxorubicin-induced cardiac damage by significantly decreasing cardiac enzymes, HIF-1α, VEGF-A, MDA, TNF-α, and caspase3 levels.
Why the study?
Doxorubicin is a chemotherapeutic agent complicated by cardiotoxic effects, but the potential protective role and mechanisms of vinpocetine in doxorubicin-induced cardiotoxicity had not been researched.
Does vinpocetine prevent doxorubicin-induced cardiotoxicity in a rat model?
Does vinpocetine prevent doxorubicin-induced cardiotoxicity in a rat model?
Vinpocetine protects against doxorubicin-induced cardiotoxicity in rats by modulating HIF/VEGF and cGMP/cAMP/SIRT signaling pathways.
Supports vinpocetine testing in doxorubicin cardiotoxicity models; leaves open translation to human cardioprotection.
Purpose: Doxorubicin (DOX) is a widely used chemotherapeutic agent complicated with cardiotoxic adverse effects. Up till now, there are no researches discussing the role of vinpocetine (VIN) in DOX cardiotoxicity. Thus, the aim of our work was to study this effect and explore the different involved mechanisms. Methods: 50 male Wistar albino rats were subjected to DOX toxicity via administration of single i.p. Dose (15 mg/kg) on the 4th day with or without co-administration of VIN (10, 20, 30 mg/kg/day) orally for 5 days. Results: Our data revealed that VIN succeeded in protecting the heart against DOX induced damage as manifested by significant decrease of cardiac enzymes, hypoxia inducible factor alpha (HIF-1α), vascular endothelial growth factor-A (VEGF-A), tissue malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α) and caspase3 levels. Furthermore, VIN given group showed marked improvement of the histopathological changes of cardiac injury, total antioxidant capacity (TAC), elevation of reduced glutathione (GSH), cyclic guanosine monophosphate (cGMP), cyclic adenosine monophosphate (cAMP) and sirtuin-1 (SIRT-1). Conclusion: We concluded that VIN could ameliorate DOX induced cardiac damage and this effect may be attributed to modulation of HIF/VEGF signaling pathway, up-regulation of cGMP/cAMP/SIRT pathway, inhibition of phosphodiesterase enzyme, besides its anti-apoptotic, anti-inflammatory, and anti-oxidant properties.
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Refaie et al. (2022) studied Doxorubicin-induced cardiotoxicity (n=50). Vinpocetine vs. Doxorubicin alone was evaluated on Cardiac enzymes, HIF-1α, VEGF-A, MDA, TNF-α, caspase3, TAC, GSH, cGMP, cAMP, SIRT-1, and histopathological changes. Vinpocetine protected against doxorubicin-induced cardiac damage by significantly decreasing cardiac enzymes, HIF-1α, VEGF-A, MDA, TNF-α, and caspase3 levels.
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