Bridelia ferruginea Inhibit Rat Heart and Liver Mitochondrial Membrane Permeability Transition Pore Opening Following Myocardial Infarction

Abstract

Despite advances in therapy, myocardial infarction (MI) remains a leading cause of death worldwide. Recently, the mitochondrion has been targeted in cardio-protection due to its role in reperfusion injury after MI. Similarly, the mitochondrion has been reported to play critical role in cardiovascular disease-associated liver dysfunctions. Medicinal plants are used in the treatment of cardiovascular diseases in Nigeria Ethnomedicine, particularly Bridelia ferruginea (BF). The study explored the effect of aqueous leaves extract of BF (AEBF) as heart and liver mitochondrial permeability transition (mPT) pore opening inhibitor using Isoprenaline-hydrochloride (ISO)-induced MI rat model. Twenty rats were used in the study, while eight were orally and daily pretreated for 14 days with 200 or 400 mg/kg of AEBF before intraperitoneal injection of ISO (100 mg/kg) for 2 days at 24 h interval. The mPT pore opening was spectrophotometrically assessed under sodium succinate energized condition at 540 nm. Results: The AEBF at 200 and 400 mg/kg decreased elevated plasmatic creatine kinase, lactate dehydrogenase and aspartate aminotransferase in ISO-induced MI in rats. Similarly, increased heart and liver lipid peroxides were inhibited by AEBF. The mPT pore opening of ISO-induced MI in rat heart was inhibited by AEBF and this impacted positively on the liver mPT pore. Furthermore, histologic examinations showed that 400 mg/kg AEBF pretreatment showed absence of lesions and necrotic cells. Conclusion: Taken together AEBF protected the heart and liver of ISO-induced MI in rats via inhibition of mPT pore opening. Hence, this may be relevant in cardio- and hepato-protection.