Cardiotoxic effects of Bisphenol-A in male Wistar rats are attenuated by Garcinia kola and its biflavonoid, kolaviron, via antioxidant and antiinflammation-based mechanisms

Abstract

Introduction

The heart, due to its high energetic metabolic and reactive oxygen production rate, is a target for oxidative stress-related injuries. Therefore, environmental toxicants such as Bisphenol-A (BPA), that exert pathologies through oxidative and nitrite stress-related mechanism may target the heart for their deleterious effects. This study was therefore designed to investigate the effect of two naturally occurring antioxidants, Garcinia kola (GK) and kolaviron, on BPA-induced cardiac dysfunction and toxicity in male Wistar rats.

Methods

Fifty-six animals were divided into 7equal groups and treated orally for 28days as follows; groups I(control) and II(vehicle) received distilled water(1.5 mL/kg) and corn oil(1.5 mL/kg) respectively. Animals in groups III-V received BPA (50 mg/kg) only, BPA + GK (200 mg/kg), BPA + kolaviron (200 m/kg) respectively, while animals in groups VI-VII received GK and kolaviron only, respectively. Thereafter, blood pressure and electrocardiogram were evaluated in each group and under anesthesia, cardiac samples were excised and analyzed for oxidative stress status, inflammatory markers and histology, respectively.

Results

BPA-only exposed rats exhibited cardiac dysfunction manifested by elevated systolic blood pressure and cardiac inflammatory markers, reduced cardiac antioxidants and distorted structural aberrations. Treatment of BPA exposed animals with either GK or kolaviron mitigated the development of these dysfunctions in varying degrees, while treatment of either GK or kolaviron alone in the absence of BPA exposure showed significant antioxidant and anti-inflammatory potentials.

Conclusion

These results suggests that Garcinia kola and its biflavonoid, kolaviron, prevents the development of bisphenol-A induced cardiac dysfunction and toxicity by potentiating antioxidant defence and impeding inflammation mediated mechanism.