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 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 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 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 Ameliorative Effect of Azadirachta Indica on Sodium Fluoride-Induced Hypertension Through Improvement of Antioxidant Defence System and Upregulation of Extracellular Signal Regulated Kinase 1/2 Signaling(Walter de Gruyter GmbH (Berlin/Boston), 2017) Omóbòwálé, T. O.; Oyagbemi, A. A.; Alaba, B. A.; Ola-Davies, O. E.; Adejumobi, O. A.; Asenuga, E. R.; Ajibade, T. O.; Adedapo, A. A.; Yakubu, M. A.Background: Toxicities due to fluoride exposure from natural and industrial sources occur commonly in man and animals with severe consequences ranging from mild cardiac derangements to sudden death. In this study, we investigated the protective effects of the methanol extract of Azadirachta indica against sodium fluoride (NaF)-induced hypertension and genotoxicity in rats. Methods: Sixty rats were divided into six groups of ten rats each as follows: Group A, the control group received distilled water; Group B rats were administered NaF at 600 ppm in drinking water; Groups C and D rats were pre-treated with the methanol extract of AI and thereafter administered NaF at 600 ppm in drinking water for 7 consecutive days; Groups E and F rats were co-administered with AI and NaF. Results: The administration of NaF caused significant (p < 0.05) increases in the blood pressure, markers of oxidative stress, serum myeloperoxidase, xanthine oxidase values in NaF-alone treated rats, compared with the control. Significant (p < 0.05) decreases were observed in cardiac and renal antioxidant defence system in rats administered NaF alone compared with the control group. NaF treatment also resulted in a reduction in the expressions of extracellular signal-regulated kinase (ERK) 1/2 in cardiac and renal tissues of NaF-treated rats. Moreover, NaF treatment elicited an increase in the frequency of micronucleated polychromatic erythrocytes when compared with the control group. Conclusions: This study shows the protective effect of AI on NaF-induced hypertension and genotoxicity through antioxidant and ERK 1/2 signaling in rats.Item Sodium fluoride induces hypertension and cardiac complications through generation of reactive oxygen species and activation of nuclear factor kappa beta(John Wiley and Sons, 2016) Oyagbemi, A. A.; Omobowale, T. O.; Asenuga, E. R.; Adejumobi, A. O.; Ajibade, T. O.; Ige, T. M.; Ogunpolu, B. S.; Adedapo, A. A.; Yakubu, M. A.Human exposure to sodium fluoride through daily use is almost inevitable, and fluoride toxicity has been associated with cardiovascular and renal dysfunction. This study investigated the mechanism of sodium fluoride (NaF)-induced hypertension and cardiovascular complications using forty male albino rats divided into four groups of ten rats each. Group A received clean tap water, while Groups B to D received graded doses of NaF in drinking water ad libitum for 10 days at concentrations of 150 ppm, 300 ppm, and 600 ppm respectively. NaF administration caused significant increases in systolic pressure, diastolic pressure, and mean arterial pressure. Markers of oxidative stress, including malondialdehyde, hydrogen peroxide, advanced oxidation protein products, and protein carbonyl, increased significantly in a dose-dependent manner in cardiac and renal tissues, alongside a significant decrease in GST activity compared to the control group. Serum markers of inflammation, cardiac injury, and renal damage such as myeloperoxidase, xanthine oxidase, blood urea nitrogen, creatinine, lactate dehydrogenase (LDH), and creatinine kinase myocardial band (CK-MB) were also significantly elevated, indicating oxidative stress as well as renal and cardiac damage after exposure. Histopathological examination of the kidney and heart revealed abnormalities in tissue architecture in NaF-treated rats, while immunohistochemistry demonstrated increased expression of nuclear factor kappa beta (NF-kB) in cardiac and renal tissues. Overall, the findings indicate that NaF induces hypertension through the generation of reactive oxygen species and activation of renal and cardiac NF-kB expression