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Browsing by Author "Ajibade, T. O."

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    Alterations in blood pressure, antioxidant status and caspase 8 expression in cobalt chloride-induced cardio-renal dysfunction are reversed by Ocimum gratissimum and gallic acid in Wistar rats
    (Elsevier GmbH, 2016) Akinrinde, A. S.; Oyagbemi, A. A.; Omobowale, T. O.; Asenuga, E. R.; Ajibade, T. O.
    The protective abilities of the chloroform extract of Ocimum gratissimum (COG) and gallic acid against cobalt chloride (CoCl2) − induced cardiac and renal toxicity were evaluated. Rats were exposed to CoCl2 (350 ppm) for 7 days, either alone, or in combination with COG (100 and 200 mg/kg) or gallic acid (120 mg/kg). CoCl2 given alone, caused significant increases (p < 0.05) in oxidative stress parameters (hydrogen peroxide, H2O2 and malondialdehyde, MDA) and increased expression of the apoptotic initiator caspase 8 in the heart and kidneys. There was significant reduction (p < 0.05) in reduced glutathione (GSH) in cardiac and renal tissues; reduction in superoxide dismutase (SOD) activity in the kidneys and adaptive increases in Glutathione S-transferase (GST) and catalase (CAT). CoCl2 also produced significant reduction (p < 0.05) in systolic (SBP), diastolic (DBP) and mean arterial (MAP) blood pressures. Oral COG and gallic acid treatment significantly reduced (p < 0.05) the levels of H2O2 and MDA; with reduced expression of caspase 8 and restoration of GSH levels, GPx, SOD and CAT activities, howbeit, to varying degrees in the heart and kidneys. COG (200 mg/kg) was most effective in restoring the blood pressures in the rats to near control levels. CoCl2-induced histopathological lesions including myocardial infarction and inflammation and renaltubular necrosis and inflammation were effectively ameliorated by the treatments administered. This study provides evidence for the protective roles of O. gratissimum and gallic acid by modulation of CoCl2-induced alterations in blood pressure, antioxidant status and pro-apoptotic caspase 8 in Wistar rats.
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    Alterations in blood pressure, antioxidant status and caspase 8expression in cobalt chloride-induced cardio-renal dysfunction arereversed by Ocimum gratissimum and gallic acid in Wistar rats
    (Elsevier B.V., 2016) Akinrinde, A. S.; Oyagbemi, A. A.; Omobowale, T. O.; Asenuga, E. R.; Ajibade, T. O.
    The protective abilities of the chloroform extract of Ocimum gratissimum (COG) and gallic acid againstcobalt chloride (CoCl2) − induced cardiac and renal toxicity were evaluated. Rats were exposed to CoCl2(350 ppm) for 7 days, either alone, or in combination with COG (100 and 200 mg/kg) or gallic acid(120 mg/kg). CoCl2given alone, caused significant increases (p < 0.05) in oxidative stress parameters(hydrogen peroxide, H2O2and malondialdehyde, MDA) and increased expression of the apoptotic initia-tor caspase 8 in the heart and kidneys. There was significant reduction (p < 0.05) in reduced glutathione(GSH) in cardiac and renal tissues; reduction in superoxide dismutase (SOD) activity in the kidneys andadaptive increases in Glutathione S-transferase (GST) and catalase (CAT). CoCl2also produced signifi-cant reduction (p < 0.05) in systolic (SBP), diastolic (DBP) and mean arterial (MAP) blood pressures. OralCOG and gallic acid treatment significantly reduced (p < 0.05) the levels of H2O2and MDA; with reducedexpression of caspase 8 and restoration of GSH levels, GPx, SOD and CAT activities, howbeit, to varyingdegrees in the heart and kidneys. COG (200 mg/kg) was most effective in restoring the blood pressures inthe rats to near control levels. CoCl2-induced histopathological lesions including myocardial infarctionand inflammation and renal tubular necrosis and inflammation were effectively ameliorated by the treat-ments administered. This study provides evidence for the protective roles of O. gratissimum and gallicacid by modulation of CoCl2-induced alterations in blood pressure, antioxidant status and pro-apoptoticcaspase 8 in Wistar rats.
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    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.
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    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.
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    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.
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    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 bioavailability
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    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.
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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.
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    Evaluation of the Effects of Alpha Evaluation of the effects of Alpha Tocopherol, Quercetin and their combination on Ethanol-Induced pancreatic and duodenal mucosal injuries: An experimental study.
    (Sciencedomain International, 2024) Akinrinde, A. S.; Ajibade, T. O.
    Aim: In this study, the effects of alpha-tocopherol (AT), quercetin (QT) or their combination on ethanol-induced pancreatic and duodenal mucosal damage were investigated in rats using morphological and biochemical evaluations. Study Design: Experimental study.Place and Duration of Study: University of Ibadan, Ibadan, Nigeria. Methodology: Ethanol-induced injuries were produced by oral administration of 40% ethanol (0.2 ml/day) for 40 consecutive days, while a control group of rats was served distilled water. Other groups received AT (2.5 mg/kg), QT (50 mg/kg) or their combination with 40% ethanol during the experimental period. Blood glucose level was significantly (p<0.05) increased in ethanol-treated rats relative to controls. Ethanol administration caused shrinkage of insulin-secreting islets tissues in the pancreas, while lesions such as erosions, loss of villi and severe inflammatory cell infiltrations of the mucosa and sub-mucosa were observed in the duodenum. These changes were accompanied by significant elevation in the levels of hydrogen peroxide (H2O2), malondialdehyde (MDA) and advanced oxidation protein products (AOPP) in the pancreas and duodenum, along with reduced activities of glutathione peroxidase (GPx) and glutathione S-transferase (GST). Treatment of rats with AT, QT, and especially their combination, yielded profound reversal of ethanol-induced effects indicated by restoration of blood glucose to control levels, preservation of pancreatic and duodenal morphology and the inhibition of ethanol-induced oxidative stress. Conclusion: Overall, dietary supplementation with AT and/or QT could potentially counteract the adverse effects associated with chronic alcohol consumption.
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    Glycine exerts renal antioxidant effects and restores hemodynamic alterations in Rats treated with Diclofenac Sodium: Roles of renal Angiotensin Converting Enzyme, Angiotensin II Receptor and Mineralocortocoid Receptor
    (Biomedical Communications Group, Ibadan, 2023) Akinrinde, A. S.; Ajibade, T. O.; Adetona, M. O.; Oyagbemi, A. A.; Adedapo, A. D. A.; Larbie, C.; Omobowale, T. O.; Ola-Davies, O. E.; Adedapo, A. A.; Saba, A. B.; Oguntibeju, O. O.; Yakubu, M. A.
    Diclofenac (DIC) is known to alter renal function in the form of hemodynamically-mediated acute renal failure. This study evaluated the protective role of the amino acid, glycine (Gly) on nephrotoxicity and acute hemodynamic alterations induced by DIC (9 mg/kg) in male Wistar rats. The rats were divided into four groups (n=7/group) including Group A (control); Group B (DIC-treated), Groups C (DIC + Gly1, 250 mg/kg) and Group D (DIC + Gly2 500 mg/kg). Systolic (SBP), diastolic (DBP) and mean arterial (MAP) blood pressures were significantly (p<0.05) reduced in rats treated with DIC alone, compared to control. Kidneys from DIC-treated rats showed altered histology with significantly (p<0.05) increased hydrogen peroxide (H2O2), malondialdehyde (MDA) and protein carbonyl contents, but decreased glutathione (GSH) glutathione peroxidase (GPx), glutathione S-transferase (GST) and superoxide dismutase (SOD) activities. Immunohistochemistry revealed down-regulation of renal angiotensin converting enzyme (ACE), but increased expressions of angiotensin type II receptor (AT2R) and mineralocorticoid receptor (MR) in DIC-treated rats. However, pre-treatment with Gly reversed most of the aforementioned effects of DIC. The present results suggest that oral glycine protected kidney tissues and restored DIC-induced hemodynamic changes by modifying renal expression of the renin-angiotensin-mineralocortocoid pathway and/or renal oxidative stress.
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    Glycine exerts renal antioxidant effects and restores hemodynamic alterations in Rats treated with Diclofenac Sodium: Roles of renal Angiotensin Converting Enzyme, Angiotensin II Receptor and Mineralocortocoid Receptor
    (Biomedical Communications Group, Ibadan, 2023) Akinrinde, A. S.; Ajibade, T. O.; Adetona, M. O.; Oyagbemi, A. A.; Adedapo, A. D. A.; Larbie, C.; Omobowale, T. O.; Ola-Davies, O. E.; Adedapo, A. A.; Saba, A. B.; Oguntibeju, O. O.; Yakubu, M. A.
    Diclofenac (DIC) is known to alter renal function in the form of hemodynamically-mediated acute renal failure. This study evaluated the protective role of the amino acid, glycine (Gly) on nephrotoxicity and acute hemodynamic alterations induced by DIC (9 mg/kg) in male Wistar rats. The rats were divided into four groups (n=7/group) including Group A (control); Group B (DIC-treated), Groups C (DIC + Gly1, 250 mg/kg) and Group D (DIC + Gly2 500 mg/kg). Systolic (SBP), diastolic (DBP) and mean arterial (MAP) blood pressures were significantly (p<0.05) reduced in rats treated with DIC alone, compared to control. Kidneys from DIC-treated rats showed altered histology with significantly (p<0.05) increased hydrogen peroxide (H2O2), malondialdehyde (MDA) and protein carbonyl contents, but decreased glutathione (GSH) glutathione peroxidase (GPx), glutathione S-transferase (GST) and superoxide dismutase (SOD) activities. Immunohistochemistry revealed down-regulation of renal angiotensin converting enzyme (ACE), but increased expressions of angiotensin type II receptor (AT2R) and mineralocorticoid receptor (MR) in DIC-treated rats. However, pre-treatment with Gly reversed most of the aforementioned effects of DIC. The present results suggest that oral glycine protected kidney tissues and restored DIC-induced hemodynamic changes by modifying renal expression of the renin-angiotensin-mineralocortocoid pathway and/or renal oxidative stress.
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    Glycine exerts renal antioxidant effects and restores hemodynamic alterations in Rats treated with Diclofenac Sodium: Roles of renal Angiotensin Converting Enzyme, Angiotensin II Receptor and Mineralocortocoid Receptor
    (Biomedical Communications Group, Ibadan, 2023) Akinrinde, A. S.; Ajibade, T. O.; Adetona, M. O.; Oyagbemi, A. A.; Adedapo, A. D. A.; Larbie, C.; Omobowale, T. O.; Ola-Davies, O. E.; Adedapo, A. A.; Saba, A. B.; Oguntibeju, O. O.; Yakubu, M. A.
    Diclofenac (DIC) is known to alter renal function in the form of hemodynamically-mediated acute renal failure. This study evaluated the protective role of the amino acid, glycine (Gly) on nephrotoxicity and acute hemodynamic alterations induced by DIC (9 mg/kg) in male Wistar rats. The rats were divided into four groups (n=7/group) including Group A (control); Group B (DIC-treated), Groups C (DIC + Gly1, 250 mg/kg) and Group D (DIC + Gly2 500 mg/kg). Systolic (SBP), diastolic (DBP) and mean arterial (MAP) blood pressures were significantly (p<0.05) reduced in rats treated with DIC alone, compared to control. Kidneys from DIC-treated rats showed altered histology with significantly (p<0.05) increased hydrogen peroxide (H2O2), malondialdehyde (MDA) and protein carbonyl contents, but decreased glutathione (GSH) glutathione peroxidase (GPx), glutathione S-transferase (GST) and superoxide dismutase (SOD) activities. Immunohistochemistry revealed down-regulation of renal angiotensin converting enzyme (ACE), but increased expressions of angiotensin type II receptor (AT2R) and mineralocorticoid receptor (MR) in DIC-treated rats. However, pre-treatment with Gly reversed most of the aforementioned effects of DIC. The present results suggest that oral glycine protected kidney tissues and restored DIC-induced hemodynamic changes by modifying renal expression of the renin-angiotensin-mineralocortocoid pathway and/or renal oxidative stress.
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    Glycine exerts renal antioxidant effects and restores hemodynamic alterations in Rats treated with Diclofenac Sodium: Roles of renal Angiotensin Converting Enzyme, Angiotensin II Receptor and Mineralocortocoid Receptor
    (Biomedical Communications Group, Ibadan, 2023) Akinrinde, A. S.; Ajibade, T. O.; Adetona, M. O.; Oyagbemi, A. A.; Adedapo, A. D. A.; Larbie, C.; Omobowale, T. O.; Ola-Davies, O. E.; Adedapo, A. A.; Saba, A. B.; Oguntibeju, O. O.; Yakubu, M. A.
    Diclofenac (DIC) is known to alter renal function in the form of hemodynamically-mediated acute renal failure. This study evaluated the protective role of the amino acid, glycine (Gly) on nephrotoxicity and acute hemodynamic alterations induced by DIC (9 mg/kg) in male Wistar rats. The rats were divided into four groups (n=7/group) including Group A (control); Group B (DIC-treated), Groups C (DIC + Gly1, 250 mg/kg) and Group D (DIC + Gly2 500 mg/kg). Systolic (SBP), diastolic (DBP) and mean arterial (MAP) blood pressures were significantly (p<0.05) reduced in rats treated with DIC alone, compared to control. Kidneys from DIC-treated rats showed altered histology with significantly (p<0.05) increased hydrogen peroxide (H2O2), malondialdehyde (MDA) and protein carbonyl contents, but decreased glutathione (GSH) glutathione peroxidase (GPx), glutathione S-transferase (GST) and superoxide dismutase (SOD) activities. Immunohistochemistry revealed down-regulation of renal angiotensin converting enzyme (ACE), but increased expressions of angiotensin type II receptor (AT2R) and mineralocorticoid receptor (MR) in DIC-treated rats. However, pre-treatment with Gly reversed most of the aforementioned effects of DIC. The present results suggest that oral glycine protected kidney tissues and restored DIC-induced hemodynamic changes by modifying renal expression of the renin-angiotensin-mineralocortocoid pathway and/or renal oxidative stress.
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    Luteolin normalizes Blood Pressure via its antioxidant activity and down-regulation of Renal Angiotensin II receptor and Mineralocorticoid receptor expressions in rats co-exposed to Diclofenac and Sodium Fluoride
    (Physiological Society of Nigeria, 2022) Ajibade, T. O.; Akinrinde, A. S.; Adetona, M. O.; Adedapo, A. D. A.; Oyagbemi, A. A.; Larbie, C.; Omobowale, T. O.; Ola-Davies, O. E.; Saba, A. B.; Adedapo, A. A.; Oguntibeju, O. O.; Yakubu, M. A.
    This study was designed to investigate the modulatory role of Luteolin (Lut), a flavonoid phytochemical, on haemodynamic parameters and the potential mechanisms involving renal Angiotensin II (AT2R) and Mineralocorticoid (MCR) receptors in renal toxicity induced by co-exposure to Diclofenac (Dcf) and sodium fluoride (NaF) in rats. Male Wistar rats were administered with either vehicle (control), Dcf only (9 mg/kg orally) or concurrently with NaF (300 ppm in drinking water). Other groups were treated with LutA (100 mg/kg) or LutB (200 mg/kg) along with Dcf and NaF exposures. All treatments lasted 8 days, following which blood pressure indices were measured using tail-cuff plethysmography. Renal expressions of AT2R and MCR were studied with immunohistochemistry, while biomarkers of oxidative and antioxidant status were also measured in the kidneys. Systolic, diastolic and mean arterial pressures were significantly (p<0.05) reduced in Dcf-treated rats, compared to control values. However, co-treatment with NaF or Lut restored these parameters. While the expression of AT2R and MCR was high in the Dcf and Dcf+NaF groups, treatment with Lut caused obvious reduction in the renal expression of these receptors. Increased lipid peroxidation (Malondialdehyde) and protein oxidation (protein carbonyls)with a lowering of reduced glutathione levels contributed to the renal toxicity of Dcf, and these were significantly ameliorated in Lut-treated rats. In conclusion, the preservation of haemodynamic indices by Luteolin in the experimental rats was probably mediated by mechanisms involving down-regulation of renal expressions of AT2R and MCR, reduction of oxidative stress and an improvement of renal antioxidant status.
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    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.
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    Preliminary studies on the haematological parameters of cockerels fed raw and processed guinea corn (Sorghum bicolor)
    (Nigerian Society for Animal Production, 2013) Soetan, K. G.; Akinrinde, A. S.; Ajibade, T. O.
    The effect of feeding raw and ground guinea com [Sorghum bicolor L. Moench) on the haematological parameters of chicken was investigated in this study. Ten (10) 6-week old cockerels were randomly divided into two groups, A and B, and were fed raw and processed (dried and ground) guinea corn, respectively, for two weeks. Packed cell volume (PCV), Haemoglobin (Hb), Red blood cell count (RBC), White blood cell, count (WBC), neutrophils, eosinophils, lymphocyte and monocyte counts were determined before and after the duration of feeding the cockerels with guinea corn. Although significant changes were not observed in most of the haematological parameters, birds fed with processed guinea corn however had a significantly higher red blood cell (RBC) count than birds fed with the raw guinea corn. These findings suggest that feeding of processed guinea corn to cockerels may be more advantageous than feeding of raw guinea corn.
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    Preliminary studies on the Haematological parameters of cockerels fed raw and processed guinea corn {sorghum bicolor)
    (Rivers State University of Sci. & Tech. Port-Harcourt., 2013) Soetan, K. O.; Akinrinde, A. S.; Ajibade, T. O.
    The effect of feeding raw and ground guinea com [Sorghum bicolor L. Moench) on the haematological parameters • of chicken was investigated in this study. Ten (10) 6-week old cockerels were randomly divided into two groups, A / and B, and were fed raw and processed (dried and ground) .guinea corn, respectively, for two weeks. Packed cel! / volume (PCV), Haemoglobin (Hb), Red blood cell count (RBC), White blood cell, count (WBC), neutrophils, : eosinophils, lymphocyte and monocyte counts were determined before and after the duration of feeding the ; •cockerels with guinea corn. Although significant changes were not observed in most of the haematological y parameters, birds,fed with processed guinea .corn however had a significantly higher red blood cel! (RBC) countlj than birds fed with the raw guinea corn. These findings suggests that feeding of processed guinea corn to cockerels may be more advantageous than feeding of raw guinea corn.
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    Saponins – A ubiquitous phytochemical: A review of its biochemical, physiological and pharmacological effects
    (Studium Press LLC, 2014) Soetan, K. O.; Ajibade, T. O.; Akinrinde, A. S.
    Saponins are ubiquitous phytochemicals widely reported to be present in many species of plants and animals. Some saponin containing plants, mainly legumes, have been used as animal feed, but others are toxic. In this review, the biochemical, physiological and pharmacological effects of saponins in humans and animals have been highlighted. Physiological and biochemical effects examined include the effects on biological membranes, gastrointestinal absorption, blood and liver cholesterol, enzymes and general body metabolism, reproductive, antioxidant and free-radical scavenging effect, smooth muscle activity and effects on ruminant digestion. Pharmacological effects of saponins such as anti-inflammatory, diuretic, hypoglycaemic, antidiabetic, antiulcer and anti-ageing effects are also examined. From the literature reviewed, it can be concluded that saponins, in general, are toxic when administered intravenously but possess a lot of therapeutic potentials especially as cytotoxic agents.
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    Saponins; a ubiquitous phytochemical: A review of its biochemical, physiological and pharmacological effects.
    (Studium Press, 2014) Soetan, K. O.; Ajibade, T. O.; Akinrinde, A. S.
    Saponins are ubiquitous phytochemicals widely reported to be present in many species of plants and animals. Some saponin containing plants, mainly legumes, have been used as animal feed, but others are toxic. In this review, the biochemical, physiological and pharmacological effects of saponins in humans and animals have been highlighted. Physiological and biochemical effects examined include the effects on biological membranes, gastrointestinal absorption, blood and liver cholesterol, enzymes and general body metabolism, reproductive, antioxidant and free-radical scavenging effect, smooth muscle activity and effects on ruminant digestion. Pharmacological effects of saponins such as anti-inflammatory, diuretic, hypoglycaemic, antidiabetic, antiulcer and anti-ageing effects are also examined. From the literature reviewed, it can be concluded that saponins, in general, are toxic when administered intravenously but possess a lot of therapeutic potentials especially as cytotoxic agents.
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    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
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