Browsing by Author "Asenuga, E."

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Enalapril confers protective effect on isoproterenol-induced myocardial infarction in rats through down regulation of cardiac troponin, c-reactive protein, upregulation of il-10β as well as anti-oxidant and anti-inflammatory activities.
(Sciencedomain International, 2018) Adeoye, B.; Ajibade, T. O.; Asenuga, E.; Adejumobi, O. A.; Oyagbemi, A. A.; Omobowale, T. O.; Adedapo, A.
Myocardial infarction is an irreversible death of heart muscle secondary due to prolonged lack of oxygen supply. The present study was designed to evaluate the protective effect of enalapril in isoproterenol-induced myocardial infarction in rats using changes in haemodynamic, biochemical, histopathological and immunohistochemistry parameters. Twenty-one male Wistar rats divided into three groups were used where the control (group A) was administered for normal saline which continued for 7 days, group B animals received normal saline for 7 days and thereafter isoproterenol (ISO) at 85 mg/kg on day 8 and 9. Group C animals were pretreated with enalapril (10 mg/kg) for 7 days and thereafter received ISO on day 8 and 9. On day 10, the blood pressure change in the animals were measured and thereafter sacrificed by cervical dislocation. The heart of each rat was removed, homogenized and used to assay for some oxidative stress markers and some antioxidant parameters. In this study, ISO caused myocardial infarction as seen by significant decrease in systolic, diastolic and mean arterial pressure but was corrected by enalapril, Enalapril caused significant increase in the levels of SOD, GPX, GST and GSH but significant decrease in MDA content and HO2 generation. But reverse was the case for group B animals. Immunohistochemistry showed that ISO caused higher expressions of cardiac C-reactive protein (CRP) and cardiac troponins 1 (CTn1) and decrease in IL-10ẞ but vice-versa for enalapril. No histopathological changes were recorded for enalapril. The study thus showed that enalapril significantly exhibits cardioprotective effects.
Protective effects of kolaviron and gallic acid against cobalt-chloride-induced cardiorenal dysfunction via suppression of oxidative stress and activation of the ERK signaling pathway
(Canadian Science Publishing, 2016) Akinrinde, S. A.; Omobowale, O.; Oyagbemi, A.; Asenuga, E.; Ajibade, T.
Cobalt (Co) toxicity is a potential public health problem due to recent renewed use of Co in orthopedic implants, dietary supplements, and blood doping in athletes and horses. We investigated the protective roles of kolaviron (KV), a bi flavonoid of Garcinia kola, and gallic acid (GA) on cobalt chloride (CoCl2)-induced cardiorenal damage in rats. CoCl2 caused significant increases (p < 0.05) in serum creatine kinase–myocardial band (CK-MB), lactate dehydrogenase (LDH), aspartate transaminase (AST), xanthine oxidase (XO), urea, creatinine, malondialdehyde, H2O2, nitric oxide, as well as C-reactive protein expression, along with significant (p < 0.05) reduction in cardiac and renal expression of extracellular signal regulated kinase (ERK) and the activities of superoxide dismutase, catalase, and glutathione S-transferase. KV and GA prevented the toxic effects of CoCl2 by stimulating ERK expression and reversing Co-induced biochemical changes. Administration of CoCl2 alone did not significantly alter ECG patterns in the rats, although co-treatment with KV (200 mg/kg) produced QT-segment prolongation and also appeared to potentiate Co hypotension. Histopathology of the heart and kidneys of rats treated with KV and GA confirmed the biochemical data. KV and GA thus protected against cardiac and renal damage in Co intoxication via antioxidant and (or) cell survival mechanisms, possibly involving ERK activation.