Related Experiment Video
Updated: Apr 21, 2026

Cardiac Spheroids as in vitro Bioengineered Heart Tissues to Study Human Heart Pathophysiology
Published on: January 23, 2021
Structural and morphological modulation of the myocardium by Dioscorea bulbifera saponins in experimentally induced
Olusola S Saka1, Omobola A Komolafe2, Oluwadare Ogunlade3
1Department of Human Anatomy, College of Medicine and Health Sciences, Afe Babalola University, Ado Ekiti, Nigeria.
Background:
This study investigated the ameliorative potential of a saponin derived from Dioscorea bulbifera bulbils in mitigating experimentally induced cardiotoxicity in adult male Wistar rats.
Methods:
Forty-eight rats were divided into eight groups (n = 6). Group A received distilled water, and Group B received doxorubicin (10 mg/kg). Groups C and D received SRF (50 or 100 mg/kg) for 14 days. Groups E and F received doxorubicin with SRF, while Groups G and H were pretreated with SRF before doxorubicin on day 15. Blood and heart tissues were collected for analysis after euthanasia.
Results:
Rats in the doxorubicin-only group (Group B) exhibited significant elevations in serum cardiac injury markers, including lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB), along with increased systolic and diastolic blood pressures and elevated malondialdehyde (MDA) levels. Conversely, activities of key antioxidant enzymes-superoxide dismutase (SOD) and catalase (CAT)-were markedly reduced. Enhanced glycogen accumulation, Caspase-3 activation, and CD4 expression further indicated heightened oxidative stress and apoptosis. Treatment with SRF, particularly in the pre- and co-administration protocols, significantly attenuated these alterations.
Conclusion:
The saponin-rich fraction of Dioscorea bulbifera bulbils demonstrated substantial cardioprotective potential against doxorubicin-induced cardiac injury, likely through its antioxidant and anti-apoptotic mechanisms.
Related Concept Videos
Cardiomyopathy II: Dilated Cardiomyopathy
Myocarditis I: Introduction
Heart Failure Drugs: Inotropic Agents
Heart Failure II: Pathophysiology

