Biochanin A attenuates doxorubicin-induced cardiotoxicity in rats with associated modulation of PI3K/Akt/mTOR and p38 MAPK signaling
By
Mashael M. AlMutairi
Huda M. AlKreathy
Rasheed A. Shaik
Amani E. Alharbi
Rania Magadmi
July 7, 2026
Clinical Scorecard: Biochanin A reduces cardiac toxicity caused by doxorubicin in rats through modulation of PI3K/Akt/mTOR and p38 MAPK pathways
At a Glance
Category Detail
Condition Cardiotoxicity due to Doxorubicin Key Mechanisms Modulation of oxidative stress, inflammation, apoptosis, and PI3K/Akt/mTOR and p38 MAPK pathways Target Population Male Wistar rats Care Setting Preclinical research
Key Highlights
Doxorubicin induces significant cardiac injury and toxicity. Biochanin A mitigates DOX-induced cardiotoxicity in a dose-dependent manner. BCA treatment improves antioxidant status and reduces inflammatory markers. Histopathological examination shows marked myocardial degeneration in DOX group. BCA alters PI3K/Akt/mTOR and p38 MAPK pathway markers. Guideline-Based Recommendations
Diagnosis
Monitor ECG parameters and serum cardiac biomarkers (CK-MB, LDH, troponin) for cardiotoxicity. Management
Consider adjunctive use of Biochanin A to reduce DOX-induced cardiac injury. Monitoring & Follow-up
Evaluate oxidative stress markers and inflammatory mediators in cardiac tissue. Risks
Doxorubicin is associated with dose-dependent cardiotoxicity. Patient & Prescribing Data
Not applicable (preclinical study in rats)
Biochanin A shows potential as a cardioprotective agent in the context of anthracycline therapy.
Clinical Best Practices
Incorporate monitoring of cardiac function in patients receiving doxorubicin. Explore natural compounds like Biochanin A for cardioprotection in chemotherapy. Related Resources & Content
