What is the clinical evidence from this study?

Study design: Other. Population: Acute doxorubicin-induced cardiotoxicity (n=32). Intervention: Vinpocetine vs. Doxorubicin alone (20 mg/kg). Primary outcome: Serum Troponin-I levels (pg/mL) (p=>0.05).

What question did this study set out to answer?

This study evaluates the potential cardioprotective effects of vinpocetine against doxorubicin-induced cardiotoxicity.

May 12, 2026Open Access

Evaluation of vinpocetine in an acute doxorubicin-induced cardiotoxicity model in rats

AEAbdullah ErcanInonu University MSMehmet Ediz SarihanInonu University OOOnural OzhanInonu University

Key Result

Vinpocetine partially modulated vascular oxidative stress parameters but did not significantly improve serum cardiac biomarkers, ECG findings, or histopathological myocardial injury in rats with acute doxorubicin-induced cardiotoxicity.

Key Points

This study evaluates the potential cardioprotective effects of vinpocetine against doxorubicin-induced cardiotoxicity.
Thirty-two male Wistar albino rats were randomly assigned to four groups: Control, DOX, VINPO, and VINPO + DOX.
DOX was administered at 20 mg/kg, and VINPO at 10 mg/kg for three days prior to assessments.
Electrocardiography, heart rate, blood pressure, and serum cardiac biomarkers were measured along with tissue analysis for oxidative stress parameters.
Doxorubicin administration resulted in significant myocardial injury and altered vascular antioxidant enzyme activities.
Vinpocetine modulated vascular SOD and CAT activities but did not significantly improve serum cardiac biomarkers or myocardial injury.
Histopathological assessments showed no significant difference in the VINPO + DOX group compared to DOX alone.

Structured PICO

Does vinpocetine prevent acute doxorubicin-induced cardiotoxicity in a rat model?

Population

32 male Wistar albino rats

Intervention

Vinpocetine (10 mg/kg for 3 days) combined with Doxorubicin (20 mg/kg, single intraperitoneal dose)

Comparator

Doxorubicin alone (20 mg/kg, single intraperitoneal dose), Vinpocetine alone, and Control

Outcome

Cardioprotective effects assessed by ECG, heart rate, blood pressure, oxygen saturation, serum cardiac biomarkers (troponin-I, CK, CK-MB), oxidative stress markers (MDA, SOD, CAT, GSH), histopathology, and caspase-3 immunoreactivitysurrogate

Vinpocetine did not demonstrate significant functional or histopathological cardioprotection against acute doxorubicin-induced cardiotoxicity in rats, despite modest effects on oxidative stress.

Main Result

Absolute Event Rate: 5681.61% vs 11580.27%

p-value: p=>0.05

Limitations

Acute model rather than chronic cardiotoxicity model
Short duration of the study
Need for more severe or longer-term cardiotoxicity models to clarify cardioprotective potential

Abstract

Doxorubicin (DOX) is an effective antineoplastic agent whose clinical use is limited by cardiotoxicity. This study aimed to evaluate the potential protective effects of vinpocetine (VINPO) in an acute DOX-induced cardiotoxicity model in rats. Thirty-two male Wistar albino rats were randomly assigned to four groups: Control, DOX (20 mg/kg, single intraperitoneal dose), VINPO (10 mg/kg for 3 days), and VINPO + DOX. Forty-eight hours after DOX administration, electrocardiography (ECG), heart rate (HR), blood pressure (BP), and oxygen saturation were recorded. Serum troponin-I, creatin kinase (CK), and CK-MB mass levels were measured. Myocardial and vascular tissues were analyzed for malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH). Histopathological and caspase-3 immunohistochemical evaluations were also performed. DOX administration resulted in significant alterations in vascular antioxidant enzyme activities and increased myocardial histopathological injury scores compared with controls. VINPO partially modulated certain oxidative stress parameters, particularly vascular SOD and CAT activities. However, serum cardiac biomarkers, ECG parameters, and caspase-3 immunoreactivity did not differ significantly among groups. Histopathological myocardial injury was not significantly improved in the VINPO + DOX group compared with DOX alone. VINPO demonstrated modest modulatory effects on selected oxidative stress parameters in acute DOX-induced cardiotoxicity. However, these effects were not consistently supported by functional or histopathological findings. Further studies using more severe or longer-term cardiotoxicity models are warranted to clarify its cardioprotective potential.

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