FACULTY OF VETERINARY MEDICINE
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Item Ameliorative Effect of Rutin on Sodium Fluoride-Induced Hypertension through Modulation of Kim-1/NF-Kb/Nrf 2 Signaling Pathways in Rats(Wiley, 2018) Oyagbemi, A. A.; Omobowale, T. O.; Ola-Davies, O. E.; Asenuga, E. R.; Ajibade, T. O.; Adejumobi, O. A.; Afolabi, J. M.; Ogunpolu, B. S.; Falayi, O. O.; Ayodeji, F.; Hassan, F. O.; Saba, A. B.; Adedapo, A. A.; Yakubu, M. A.Sodium fluoride is one of the neglected environmental contaminants. Inorganic fluorides in the environment are found in the air, water, and land. In the study, forty male Wistar albino rats were randomly divided into four groups with 10 rats in a group. Group A was the control group which was given normal saline, Group B was exposed to 300 ppm of Sodium fluoride in drinking water, while Groups C and D received Sodium fluoride along with Rutin (100 mg/kg and 200 mg/kg) orally daily for a week. Administration of Sodium fluoride alone led to significant increases in blood pressure and decreased serum nitric oxide. Immunohistochemistry revealed higher expressions of kidney injury molecule 1 (Kim-1), nuclear factor kappa beta (NF-κB), and downregulation of nuclear factor erythroid 2-related factor 2 (Nrf2) in rats administered Sodium fluoride. Rutin co-treatment with Sodium fluoride normalized blood pressure, lowered Kim-1 and NF-κB expressions, and improved nitric oxide bioavailabilityItem Ameliorative Effect of Garlic Acid on Doxorubicin-Induced Cardiac Dysfunction in Rats(Walter de Gruyter GmbH, 2018) Omobowale, T. O.; Oyagbemi, A. A.; Folasire, A. M.; Ajibade, T. O.; Asenuga, E. R.; Adejumobi, O. A.; Ola-Davies, O. E.; Oyetola, O.; James, G.; Adedapo, A. A.; Yakubu, M. A.Background: The use of doxorubicin (DOX) as an anti- neoplastic agent has been greatly limited because of the myriad of toxic sequelae associated with it. The aim of this study was to assess the protective effects of gallic acid (GA) on DOX-induced cardiac toxicity in rats. Methods: Sixty male rats (Wistar strain) were used in this study. They were divided into six groups (A-F) each containing 10 animals. Group A was the control. Rats in Groups B, C, and D were treated with DOX at the dosage of 15 mg/kg body weight i.p. Prior to this treatment, rats in Groups C and D had been treated orally with GA for 7 days at the dosage of 60 and 120 mg/kg, respectively. Animals from Groups E and F received only 60 and 120 mg/kg GA, respectively, which were administered orally for 7 days Results: The exposure of rats to DOX led to a significant Received December 27, 2016; accepted July 23, 2017; previously (p<0.05) decrease in the cardiac antioxidant defence published online October 9, 2017 Abstract Background: The use of doxorubicin (DOX) as an anti- neoplastic agent has been greatly limited because of the myriad of toxic sequelae associated with it. The aim of this study was to assess the protective effects of gallic acid (GA) on DOX-induced cardiac toxicity in rats. Conclusions: The GA pretreatment significantly alleviated GA-associated ECG abnormalities, restored the antioxi dant status and prevented cardiac damage.Item 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.Item Ameliorative effect of gallic acid on doxorubicin-induced cardiac dysfunction in rats(De Gruyter, 2017) Omobowale, T. O.; Oyagbemi, A. A.; Folasire, A. F.; Ajibade, T. O.; Asentiga, E. R.; Adejumobi, O. A.; Ola-Davies, O. E.; Oyetola, O.; James, G.; Adedapo, A. A.; Yakubu, M. A.Background: The use of doxorubicin (DOX) as an antineoplastic agent has been greatly limited because of the myriad of toxic sequelae associated with it. The aim of this study was to assess the protective effects of gallic acid (GA) on DOX-induced cardiac toxicity in rats. Methods: Sixty male rats (Wistar strain) were used in this study. They were divided into six groups (A–F) each containing 10 animals. Group A was the control. Rats in Groups B, C, and D were treated with DOX at the dosage of 15 mg/kg body weight i.p. Prior to this treatment, rats in Groups C and D had been treated orally with GA for 7 days at the dosage of 60 and 120 mg/kg, respectively. Animals from Groups E and F received only 60 and 120 mg/kg GA, respectively, which were administered orally for 7 days. Results: The exposure of rats to DOX led to a significant (p 0.05) decrease in the cardiac antioxidant defence system and elevation of creatine kinase myocardial band and lactate dehydrogenase. The electrocardiography results showed a significant decrease in heart rate, QRS, and QT-segment prolongation. GA alone improved the antioxidant defence system. Conclusions: The GA pretreatment significantly alleviated GA-associated ECG abnormalities, restored the antioxidant status and prevented cardiac damage.