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 Luteonin-mediated Km-1 / NF-kB / Nrf2 Signaling Pathways Protects Sodium Fluoride Induced Hypertension and Cardiovascular Complications. Biofactors.(Wiley-Blackwell, 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.; Saba, A. B.; Adedapo, A. A.; Yakubu, M. A.The use of sodium fluoride (NaF) as a major ingredient for toothpaste, mouth wash, and mouth rinse has become inevitable in our day-to-day life. However, flavonoids such as Luteolin might be of great value in the prevention of toxicity associated with accidental or inevitable ingestion of NaF. In the study, 40 male Wistar albino rats were randomly divided into four groups with 10 rats in a group. Group A was the control group and received normal saline, Group B was exposed to NaF at 300 ppm (300 mg/L) in drinking water daily for a week, Groups C and D were exposed to 300 ppm (300 mg/L) of NaF and co-administered with Luteolin orally daily at a dosage of 100 mg/kg and 200 mg/kg for the same time point. Our results indicated that NaF caused significant increases in systolic blood pressure, diastolic blood pressure, mean arterial pressure, malondialdehyde, protein carbonyl, myeloperoxidase, advanced oxidative protein products, together with significant reductions in glutathione peroxidase, superoxide dismutase, catalase, glutathione reductase, reduced glutathione, and nitric oxide (NO) bioavailability. The electrocardiogram results showed that NaF alone caused significant prolongation of QT and QTc intervals. Immunohistochemistry revealed that NaF caused increase expressions of Kidney injury marker 1 (Kim-1), nuclear factor kappa beta (NF-κB), nuclear factor erythroid 2-related factors 2 (Nrf2), and cardiac troponin I (CTnI). Together, Luteolin co-administration with NaF improved NO bioavailability, reduced high blood pressure, markers of oxidative stress, reversed prolongation of QT and QTc intervals, and lowered the expressions of Kim-1, NF-κB, and CTnI.Item Protective Effect of Azadirachtha inidica and Vitamin E against Arsenic Acid- Induced Genotoxicity and Apoptosis in Rats(Taylor & Francis, 2018) Oyagbemi, A. A.; Omobowale, T. O.; Ola-Davies, O. E.; Adejumobi, O. A.Sodium arsenite is one of the major environmental toxicants with severe toxicological consequences in some developing and developed countries. Rats in Group A received normal saline. Genotoxicity and apoptosis were induced by single intraperitoneal injection of 10 mg/kg Sodium arsenite to rats in Groups B-F. Rats in Groups C and D had earlier been pretreated with Azadirachta indica (100 and 200 mg/kg) or E and F with vitamin E (50 and 100 mg/kg), respectively. Markers of oxidative stress, inflammation, hepatic damage, genotoxicity, and apoptosis were assessed. Pretreatment of rats with either Azadirachta indica or vitamin E led to a significant increase in the activities of glutathione S-transferase (GST), catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH) in the liver compared to the group that received Sodium arsenite alone. Markers of oxidative stress and inflammation, malondialdehyde (MDA), hydrogen peroxide (H₂O₂) generation, nitric oxide (NO), and myeloperoxidase (MPO), were significantly lowered in rats pretreated with Azadirachta indica or vitamin E. The frequency of micronucleated polychromatic erythrocytes (MNPCEs) and expression of caspase-3 were significantly reduced in rats pretreated with either Azadirachta indica or vitamin E compared to rats intoxicated with arsenite. Histopathology of the liver showed areas of infiltration of inflammatory cells with death of numerous hepatocytes in Sodium arsenite intoxicated rats, and these were reversed by Azadirachta indica. Together, this study reports the genoprotective and antiapoptotic effect of Azadirachta indica by significant reduction in micronuclei formation, apoptosis, and oxidative stress induced by arsenic intoxication.Item Antihypertensive Effect of Poly phenol Rich fraction of Azadirachta Indica on Nw-Nitro-L-Arginine Methyl Esther-Induced Hypertension and Cardiovenal Dysfunction(Georg Thieme Verlag KG, 2018) Omobowale, T. O.; Oyagbemi, A. A.; Ogunpolu, B. S.; Oladavies, O. E.; Olukunle, J. O.; Asenuga, E. R.; Ajibade, T. O.; Adejumobi, O. A.; Afolabi, J. M.; Faloju, O. O.; Ashafa, A.; Adedapo, A. A.; Yakubu, M. A.Azadirachta indica (Al) is a medicinal plant with reported anti-oxidant and cardio-protective properties. The use of plant-based polyphenols has become greatly increased in the last one decade. The present study investigated the protective effect of the polyphenol-rich fraction (PRF) of the methanol-extract of Azadirachta indica against N-Nitro-L-Arginine Methyl Ester induced Hypertension and cardiorenal dysfunction in rats. Fifty (50) Wistar albino rats were grouped into five groups. Group A, the control, was administered potable water. Groups B-E received orally, 40 mg/kg of L-NAME only, 40 mg/kg of L-NAME and 100 mg/kg of Al extract, 40 mg/kg of L-NAME and 200 mg/kg of Al extract, and 40 mg/kg of L-NAME and 25 mg/kg of Captopril, respectively for 21 days. The results of the present study revealed that L-NAME administration led to a significant increase in systolic blood pressure, diastolic blood pressure, and mean arterial blood pressure. Markers of oxidative stress (malondialdehyde, protein carbonyl) increased significantly while there was reduction in reduced glutathione level, activities of superoxide dismutase, glutathione peroxidase and glutathione-S-transferase as well nitric oxide bioavailability. Immunohistochemistry revealed higher expressions of nuclear factor kappa beta (NF-kB) and kidney injury molecule 1 (Kim-1) and lower expressions of nuclear factor erythroid 2-related factor 2 (Nrf2) in hypertensive rats. Our results indicated that with PRF of Azadirachta indica restored high blood pressure, reduced markers of oxidative stress, normalized serum nitric oxide bioavailability and increased the expressions of Nrf2. Hence, PRF of Azadirachta indica could be used for the treatment of Hypertension.Item Osteodystrophia fibrosa secondary to a chronic renal failure in a dog. a case report(Faculty of Veterinary Medicine, University of Ibadan, 2018) Adejumobi, O. A.; Omobowale, T. O.; Alaka, O. O.A five year male Rottweiler was presented to the Small animal clinic of the Veterinary Teaching Hospital. University of Ibadan, being a referral from Lagos. Bilateral swelling and deformity of the skull bones were observed. Palpation revealed swollen gums and weak mobile teeth weak. Urination was frequent and the urine very clear. Haematology and blood chemistry revealed non-regenerative anaemia, mild leucopenia, hypocalcaemia, hyper-phosphataemia, high serum blood urea and creatinine, and hyper-bilirubinaemia. Treatment was instituted with dextrose saline to rehydrate the animal and correct electrolyte and metabolic disorders. The dog however died despite intervention. At post mortem, the carcass was found to be jaundiced, the premolars were mal-positioned. Calcification was visible on the lower jaw. Kidneys were small, firm, with many white specks on the cortical surface. A diagnosis of Uremic renal failure with Osteodystrophia fibrosa (renal rickets) was made. The possible causes and clinical implications of the condition were discussed.Item Reduction in Nitric Oxide Bioavailability Shifts Serum Lipid Content Towards Atherogenic Lipoprotein in Rats. Biomedicine and pharmacotherapy(Elsevier, 2018) Aluko, E. O.; Omobowale, T. O.; Oyagbemi, A. A.; Adejumobi, O. A.; Fasanmade, A. A.Nitric oxide (NO) is major endothelial relaxing factor and reduction in its bioavailabilty has been linked to hypertension. Furthermore, high lipid content is a strong risk factor predisposing to cardiovascular diseases. The principal focus of this study was to investigate the effect of blockade of nitric oxide synthase (NUS) on serum lipid content in rats. Male Wistar rats (150-170g, a 15) were randomly divided into two gruupe designated control (n=5), and L-Name group (n-10) and were gavage with distilled water and 60 mg/kg of L-NAME respectively daily for three weeks. After 3 weeks, the L-NAME group was sub-divided into two sub-groups (n=5 each): 1-NAME (00 mg/kg of L-NAME), and L-NAME plus ramipril (LR) (60 mg/kg of L-NAME plus 20 mg/kg of ramipril) and were treated daily for another three weeks. The blood pressure (BP) of the conscious rats was measured by tail-cuft method at the onset, at the third and at the sixth weeks of the experiment; while serum lipid contents and NO were measured at the third and sixth weeks. At the end of the experiment blood sample was drawn by ocular puncture for evaluation of lipid profile and NO, and the animals were later euthanized by overdere of anesthesia. Data were analyzed using ANOVA at p < 0.05. There was a significant increase in HP, triglyceride, total cholesterol, low density lipoprotein-cholesterol, and atherogenic indices in L-NAME group compared to the control and LR group (p<0.05); NO and high density lipoprotein cholesterol was significant lower in the L-NAME group compared to contral and LR (p<0.05). In conclusion, reduction in NO bioavail- ability alters lipid metabolism, which was rected by ramiprilItem 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 Hepatotoxicity in Wistar Rats Through Antioxidant Defence System(Taylor & Francis, 2018) Omobowale, T. O.; Oyagbemi, A. A.; Ajufo, U. E.; Adejumobi, O. A.; Ola-Davies, O. E.; Adedapo, A. A.; Yakubu, M. A.Hepatotoxicity has been found to be one of the main side effects asso- ciated with doxorubicin (Dox) administration in cancer therapy. The aim of the present study was to examine the ameliorative effect of gallic acid (GA) in Dox-induced hepatotoxicity. Sixty male Wistar rats of 10 rats per group were used in this study and were randomly divided into 6 experimental groups (A-F). Rats in Group A served as the control group and received distilled water orally for 7 days: Group B was given Dox at 15 mg/kg body weight intraperitoneally (IP) on Day 8. Group C was given GA at 60 mg/kg body weight orally for 7 days + Dox at 15 mg/kg IP on Day 8. Group D was given GA at 120 mg/kg body weight orally for 7 days +Dox at 15 mg/kg IP on day 8. Rats in Groups E and F were administered GA alone at 60 and 120 mg/kg body weight orally for 7 days, respectively. Dox administration led to a significant reduction in hepatic reduced glu- tathione and nonprotein thiol (NPT) together with significant increase in hepatic malondialdehyde, hydrogen peroxide generation, superax- ide dismutase, and catalase activity; hepatic glutathione peroxidase and glutathione-S-transferase activity were significantly inhibited in Dox-treated rats, The serum alanine aminotransferase (ALT), alkaline phosphatase, and total bilirubin concentrations were significantly ele- vated following Dox administration. Pretreatment with GA ameliorated Dox-induced hepatotoxicity and oxidative stress. The results suggest that GA may offer protection against hepatic damage in Dox cancer chemotherapy.Item Effect of Arsenic Acid Withdrawal on Hepatoxicity and Disruptor of Erythrocyte Antioxidant Defense System(Elsevier B.V, 2017) Oyagbemi, A. A.; Omobowale, T. O.; Adenuga, E. R.; Afolabi, J. M.; Adejumobi, O. A.; Adedapo, A. A.; Yakubu, M. A.We investigated the effects of withdrawal from Sodium arsenite (NaAsO2) on the hepatic and antioxidant defense system in male Wistar rats using a before and after texicant design. Rats were orally gavaged daily with varying duses of NaAsO fur a period of 4 weeks. One half of the population was sacrificed and the remaining half had the toxicant withdrawn for anodier ferther 4 weeks. Biochemical and immunohistochemical techniques were used to assess the impact of withdrawal on the erythrocyte and hepatic systems. Exposure of Wistar rats to NaASO, led to a significant (p<0.05) increase in hepatic and erythrocyte markers of oxidative stress (malondialdehyde, thiol contents and hydrogen peroxide generation). Concurrently, there was a significant (p < 0.05) increase in hepatic and erythrocyte antioxidant enzymes (glutathione-S-transferase, glutathione peroxidase and superoxide dismutase) following exposure. Withdrawal from NaAsO exposure led to a decline in both erythrocyte and hepatic markers of oxidative stress and together with a significant improvement in antioxidant defense system. Histopathology and immunohistochemistry revealed varying degrees of recovery in hepatocyte ultrastructure alongside increased expression of the pre-survival protein Kinase B (Akt/PKB) after 4 weeks of NAO with drawal. Conclusively, withdrawal from exposure led to a partial recovery from uxidative stress-mediated he patotoxicity and derangements in erythrocyte antioxidant system through Akt/PKB pathway.