26 results on '"Blessing Seun Ogunpolu"'
Search Results
2. Effect of cocoa powder on hypertension and antioxidant status in uninephrectomized hypertensive rats
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Olayinka Christianah Jayeola, Ademola Adetokunbo Oyagbemi, Omolara Ibiwunmi Okunlola, Olayiwola Olubamiwa, Temidayo Olutayo Omobowale, Temitayo Olabisi Ajibade, Foluso Bolawaye Bolaji-Alabi, Blessing Seun Ogunpolu, Olufunke Olubunmi Falayi, Adebowale Benard Saba, Adeolu Alex Adedapo, Momoh Audu Yakubu, Afolabi Oluwadun, and Oluwafemi Omoniyi Oguntibeju
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antioxidant therapy ,cocoa powder ,high salt diet ,hypertension ,oxidative stress ,Animal culture ,SF1-1100 ,Veterinary medicine ,SF600-1100 - Abstract
Background and Aim: High salt diet and uninephrectomy are associated with high blood pressure with attendant cardiovascular disease conditions such as hypertension, renal damage, myocardial infarction, and stroke. The aim of this study was to investigate the beneficial effects of consumption of cocoa and cocoa-containing products in the management of high blood pressure in uninephrectomized hypertensive rats. Materials and Methods: The effect of cocoa powder on blood pressure, markers of inflammation, oxidative stress, and histopathology were investigated in uninephrectomized animals fed with cocoa feed alone or in combination with a high salt diet. Male rats were randomly divided into five groups: Group A was the control group and fed with normal feed alone, Group B was fed with cocoa feed alone, Group C was fed with high salt diet (8% salt), Group D was fed with cocoa-feed compounded with 8% salt for 4 weeks after uninephrectomy, and Group E was uninephrectomized rats on a normal diet. The left kidneys of animals in Groups C, D, and E were removed by surgery. After 4 weeks of treatment, the systolic, diastolic, and mean arterial blood pressure was measured. The serum markers of renal damage and oxidative stress were determined. Histological examination was also performed on renal and cardiac tissues. Results: Results showed significant increases in biomarkers of oxidative stress, inflammation, and renal damage with a concomitant decrease in antioxidant status in hypertensive uninephrectomized rats. Cocoa feed, however, significantly improved blood pressure and nitric oxide bioavailability, antioxidant status and reduced markers of inflammation and oxidative stress. Conclusion: These findings show that cocoa powder could be used to maintain blood pressure levels in hypertensive rats through its antioxidant capacity.
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- 2020
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3. Effect of cocoa powder on hypertension and antioxidant status in uninephrectomized hypertensive rats
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Ademola Adetokunbo Oyagbemi, Olayiwola Olubamiwa, Olayinka Christianah Jayeola, Temitayo Olabisi Ajibade, Olufunke Olubunmi Falayi, Omolara Ibiwunmi Okunlola, Momoh A. Yakubu, Adeolu Alex Adedapo, Adebowale Benard Saba, Temidayo Olutayo Omobowale, Foluso Bolawaye Bolaji-Alabi, Oluwafemi Omoniyi Oguntibeju, Blessing Seun Ogunpolu, and Afolabi Oluwadun
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medicine.medical_specialty ,Antioxidant ,hypertension ,Normal diet ,030309 nutrition & dietetics ,medicine.medical_treatment ,Veterinary medicine ,Diastole ,high salt diet ,030204 cardiovascular system & hematology ,medicine.disease_cause ,SF1-1100 ,Nitric oxide ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Internal medicine ,SF600-1100 ,medicine ,oxidative stress ,Myocardial infarction ,Stroke ,0303 health sciences ,General Veterinary ,business.industry ,food and beverages ,medicine.disease ,Animal culture ,Blood pressure ,Endocrinology ,chemistry ,cocoa powder ,antioxidant therapy ,business ,Oxidative stress ,Research Article - Abstract
Background and Aim: High salt diet and uninephrectomy are associated with high blood pressure with attendant cardiovascular disease conditions such as hypertension, renal damage, myocardial infarction, and stroke. The aim of this study was to investigate the beneficial effects of consumption of cocoa and cocoa-containing products in the management of high blood pressure in uninephrectomized hypertensive rats. Materials and Methods: The effect of cocoa powder on blood pressure, markers of inflammation, oxidative stress, and histopathology were investigated in uninephrectomized animals fed with cocoa feed alone or in combination with a high salt diet. Male rats were randomly divided into five groups: Group A was the control group and fed with normal feed alone, Group B was fed with cocoa feed alone, Group C was fed with high salt diet (8% salt), Group D was fed with cocoa-feed compounded with 8% salt for 4 weeks after uninephrectomy, and Group E was uninephrectomized rats on a normal diet. The left kidneys of animals in Groups C, D, and E were removed by surgery. After 4 weeks of treatment, the systolic, diastolic, and mean arterial blood pressure was measured. The serum markers of renal damage and oxidative stress were determined. Histological examination was also performed on renal and cardiac tissues. Results: Results showed significant increases in biomarkers of oxidative stress, inflammation, and renal damage with a concomitant decrease in antioxidant status in hypertensive uninephrectomized rats. Cocoa feed, however, significantly improved blood pressure and nitric oxide bioavailability, antioxidant status and reduced markers of inflammation and oxidative stress. Conclusion: These findings show that cocoa powder could be used to maintain blood pressure levels in hypertensive rats through its antioxidant capacity.
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- 2020
4. Clofibrate, a PPAR‐α agonist, abrogates sodium fluoride‐induced neuroinflammation, oxidative stress, and motor incoordination via modulation of GFAP/Iba‐1/anti‐calbindin signaling pathways
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Fasilat Oluwakemi Hassan, James O. Olopade, Olufunke Olubunmi Falayi, Oluwabusayo R Folarin, Lyndy Joy McGaw, Temidayo Olutayo Omobowale, Kabirat Adigun, Momoh A. Yakubu, Olumuyiwa Abiola Adejumobi, Olamide E. Adebiyi, Ebunoluwa Rachael Asenuga, Adeolu Alex Adedapo, Ademola Adetokunbo Oyagbemi, Blessing Seun Ogunpolu, Adedeji K Adebayo, Sanah M. Nkadimeng, Oluwafemi Omoniyi Oguntibeju, Olufunke Eunice Ola-Davies, and Adebowale Bernard Saba
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Male ,Agonist ,Calbindins ,medicine.drug_class ,Health, Toxicology and Mutagenesis ,010501 environmental sciences ,Management, Monitoring, Policy and Law ,Pharmacology ,Toxicology ,medicine.disease_cause ,01 natural sciences ,Neuroprotection ,Fluorides ,Random Allocation ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Glial Fibrillary Acidic Protein ,Sodium fluoride ,medicine ,Animals ,PPAR alpha ,Clofibrate ,Rats, Wistar ,Neuroinflammation ,0105 earth and related environmental sciences ,Inflammation ,Glial fibrillary acidic protein ,biology ,Chemistry ,Calcium-Binding Proteins ,Microfilament Proteins ,General Medicine ,Rats ,Oxidative Stress ,Neuroprotective Agents ,030220 oncology & carcinogenesis ,Toxicity ,biology.protein ,Sodium Fluoride ,Ataxia ,Biomarkers ,Oxidative stress ,Signal Transduction ,medicine.drug - Abstract
Fluoride is an environmental contaminant that is ubiquitously present in air, water, and soil. It is commonly added in minute quantity to drinking water, toothpaste, and mouth rinses to prevent tooth decay. Epidemiological findings have demonstrated that exposure to fluoride induced neurodevelopmental toxicity, developmental neurotoxicity, and motor disorders. The neuroprotective effect of clofibrate, a peroxisome proliferator-activated receptor alpha agonist, was investigated in the present study. Forty male Wistar rats were used for this study and randomly grouped into 10 rats per group as control, sodium fluoride (NaF) alone (300 ppm), NaF plus clofibrate (250 mg/kg), and NaF plus lisinopril (10 mg/kg), respectively, for 7 days. NaF was administered in drinking water while clofibrate and lisinopril were administered by oral gavage. Markers of neuronal inflammation and oxidative stress, acetylcholinesterase activity, and neurobehavioral (hanging wire and open field) tests were performed. Immunohistochemistry was performed on brain tissues, and they were probed with glial fibrillary acidic protein, ionized calcium-binding adaptor molecule 1, and cerebellar Ca2+ -binding protein calbindin-D28k. The results showed that NaF significantly increased of oxidative stress and neuroinflammation and inhibited AChE activity. Immunostaining showed reactive astrocytes, microgliosis, loss of dendritic spines, and arborization in Purkinje cells in rats administered only NaF. Neurobehavioral results showed that cotreatment of NaF with clofibrate improved muscular strength and locomotion, reduced anxiety, and significantly reduced astrocytic count. Overall, cotreatment of NaF with either clofibrate or lisinopril showed neuroprotective effects by mitigating neuronal inflammation and oxidative and motor incoordination. Hence, clofibrate could be seen as a novel drug candidate against neurodegeneration and motor disorders.
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- 2019
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5. Clofibrate, a Peroxisome Proliferator-Activated Receptor-Alpha (PPARα) Agonist, and Its Molecular Mechanisms of Action against Sodium Fluoride-Induced Toxicity
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Ademola Adetokunbo, Oyagbemi, Olumuyiwa Abiola, Adejumobi, Theophilus Aghogho, Jarikre, Olumide Samuel, Ajani, Ebunoluwa Racheal, Asenuga, Idayat Titilayo, Gbadamosi, Aduragbenro Deborah A, Adedapo, Abimbola Obemisola, Aro, Blessing Seun, Ogunpolu, Fasilat Oluwakemi, Hassan, Olufunke Olubunmi, Falayi, Iyanuoluwa Omolola, Ogunmiluyi, Temidayo Olutayo, Omobowale, Oluwatosin Adetola, Arojojoye, Olufunke Eunice, Ola-Davies, Adebowale Benard, Saba, Adeolu Alex, Adedapo, Benjamin Obukowho, Emikpe, Matthew Olugbenga, Oyeyemi, Sanah Malomile, Nkadimeng, Lyndy Joy, McGaw, Prudence Ngalula, Kayoka-Kabongo, Oluwafemi Omoniyi, Oguntibeju, and Momoh Audu, Yakubu
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Male ,Oxidative Stress ,Animals ,Sodium Fluoride ,PPAR alpha ,Clofibrate ,Dental Caries ,Rats, Wistar ,Rats - Abstract
Sodium fluoride (NaF) is one of the neglected environmental pollutants. It is ubiquitously found in the soil, water, and environment. Interestingly, fluoride has been extensively utilized for prevention of dental caries and tartar formation, and may be added to mouthwash, mouth rinse, and toothpastes. This study is aimed at mitigating fluoride-induced hypertension and nephrotoxicity with clofibrate, a peroxisome proliferator-activated receptor-alpha (PPARα) agonist. For this study, forty male Wistar rats were used and randomly grouped into ten rats per group, control, sodium fluoride (NaF; 300 ppm) only, NaF plus clofibrate (250 mg/kg) and NaF plus lisinopril (10 mg/kg), respectively, for 7 days. The administration of NaF was by drinking water ad libitum, while clofibrate and lisinopril were administered by oral gavage. Administration of NaF induced hypertension, and was accompanied with exaggerated oxidative stress; depletion of antioxidant defence system; reduced nitric oxide production; increased systolic, diastolic and mean arterial pressure; activation of angiotensin-converting enzyme activity and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB); and testicular apoptosis. Treatment of rats with clofibrate reduced oxidative stress, improved antioxidant status, lowered high blood pressure through the inhibition of angiotensin-converting enzyme activity, mineralocorticoid receptor over-activation, and abrogated testicular apoptosis. Taken together, clofibrate could offer exceptional therapeutic benefit in mitigating toxicity associated with sodium fluoride.
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- 2021
6. Luteolin Attenuates Glycerol-Induced Acute Renal Failure and Cardiac Complications Through Modulation of Kim-1/NF-κB/Nrf2 Signaling Pathways
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Ebunoluwa Racheal Asenuga, Adebowale Benard Saba, Oluwafemi Omoniyi Oguntibeju, Temitayo Olabisi Ajibade, Temidayo Olutayo Omobowale, Momoh A. Yakubu, Olumuyiwa Abiola Adejumobi, Olufunke Eunice Ola-Davies, Jeremiah Moyinoluwa Afolabi, Adeolu Alex Adedapo, Ademola Adetokunbo Oyagbemi, Blessing Seun Ogunpolu, Fasilat Oluwakemi Hassan, Enivwenaye Williams Nabofa, and Olufunke Olubunmi Falayi
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0301 basic medicine ,Glycerol ,Male ,NF-E2-Related Factor 2 ,Kidney ,03 medical and health sciences ,High morbidity ,chemistry.chemical_compound ,0302 clinical medicine ,Medicine ,Animals ,Pharmacology (medical) ,Rats, Wistar ,Luteolin ,030109 nutrition & dietetics ,Nutrition and Dietetics ,business.industry ,NF-kappa B ,NF-κB ,030229 sport sciences ,Acute Kidney Injury ,Rats ,Oxidative Stress ,chemistry ,Cancer research ,business ,Cell Adhesion Molecules ,Food Science ,Nrf2 signaling ,Signal Transduction - Abstract
Acute renal failure (ARF) has been documented as a life-threatening disease with high morbidity and mortality. We investigated the protective effect of Luteolin against ARF. In this study, forty-male Wistar albino rats were randomly divided into four groups (
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- 2020
7. Luteolin mitigates potassium dichromate-induced nephrotoxicity, cardiotoxicity and genotoxicity through modulation of Kim-1/Nrf2 signaling pathways
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Oluwafemi Omoniyi Oguntibeju, Blessing Seun Ogunpolu, Yemisi Dorcas Adeoye, Temidayo Olutayo Omobowale, Fasilat Oluwakemi Hassan, Idayat Titilayo Gbadamosi, Olufunke Eunice Ola-Davies, Adebowale Benard Saba, Momoh A. Yakubu, Ebunoluwa Rachael Asenuga, Ademola Adetokunbo Oyagbemi, Oluwatosin Adetola Arojojoye, Omolola Victoria Awoyomi, Temitayo Olabisi Ajibade, Adeolu Alex Adedapo, and Olufunke Olubunmi Falayi
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Antioxidant ,NF-E2-Related Factor 2 ,Health, Toxicology and Mutagenesis ,medicine.medical_treatment ,Management, Monitoring, Policy and Law ,Pharmacology ,Toxicology ,medicine.disease_cause ,Kidney ,Antioxidants ,Nephrotoxicity ,Nitric oxide ,chemistry.chemical_compound ,medicine ,Animals ,Luteolin ,Potassium dichromate ,Cardiotoxicity ,Chemistry ,General Medicine ,Rats ,Oxidative Stress ,medicine.anatomical_structure ,Potassium Dichromate ,Oxidative stress - Abstract
Environmental and occupational exposure to chromium compounds has become potential aetiologic agent for kidney disease with excessive generation of free radicals, apoptosis, and inflammatory. These pathophysiologic mechanisms of potassium dichromate (K2 Cr2 O7 ) have been well correlated with nephrotoxicity and cardiotoxicity. The cardioprotective and nephroprotective effects of Luteolin, a known potent antioxidant were evaluated in this study with 40 healthy rats in four experimental groups: Group A (normal saline), Groups B (30 mg/kg K2 Cr2 O7 ), Group C (Luteolin 100 mg/kg and K2 Cr2 O7 30 mg/kg), and Group D (Luteolin 200 mg/kg and K2 Cr2 O7 30 mg/kg), respectively. Markers of antioxidant defense system, oxidative stress, blood pressure and micronucleated polychromatic erythrocytes (MnPEs), immunohistochemistry of Kidney, injury molecule (Kim-1), nuclear factor erythroid 2-related factor 2 (Nrf2), and cardiac troponin I were determined. Administration of K2 Cr2 O7 increased blood pressure parameters in systolic, diastolic and mean arterial blood pressures, markers of oxidative stress, and frequency of micronucleated polychromatic erythrocytes, together with reduction in serum nitric oxide level. Renal Kim-1 and cardiac troponin I expressions were higher, but lower expressions of renal and cardiac Nrf2 were recorded with immunohistochemical analysis. Pre-treatment with Luteolin restored blood pressure parameters, with concomitant reduction in oxidative stress indicators, augmented antioxidant mechanisms and serum Nitric oxide level, lowered the expressions of Kim-1, cardiac troponin I and up-regulated of both cardiac and renal Nrf2, reduced the frequency of micronucleated polychromatic erythrocytes. Taken together, this study therefore demonstrates the cardioprotective, nephro protective and antigenotoxic effects of Luteolin through antioxidantive and radical scavenging mechanisms.
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- 2020
8. Ramipril blunts glycerol-induced acute renal failure in rats through its antiapoptosis, anti-inflammatory, antioxidant, and renin-inhibiting properties
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Adeolu Alex Adedapo, Ademola Adetokunbo Oyagbemi, Momoh A. Yakubu, Blessing Seun Ogunpolu, Oluwafemi Omoniyi Oguntibeju, Olufunke Olubunmi Falayi, Ehizogie Ruth Osaretin, and Temidayo Olutayo Omobowale
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Ramipril ,Glycerol ,Physiology ,030232 urology & nephrology ,Anti-Inflammatory Agents ,Apoptosis ,Pharmacology ,medicine.disease_cause ,Antioxidants ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Drug Discovery ,Renin–angiotensin system ,Renin ,medicine ,Animals ,Blood urea nitrogen ,030304 developmental biology ,0303 health sciences ,Creatinine ,Kidney ,business.industry ,Acute kidney injury ,General Medicine ,Acute Kidney Injury ,medicine.disease ,Rats ,Disease Models, Animal ,Oxidative Stress ,medicine.anatomical_structure ,chemistry ,Inflammation Mediators ,business ,Pioglitazone ,Oxidative stress ,medicine.drug - Abstract
Objectives Acute kidney injury (AKI) is a malady with a sudden onset resulting in buildup of waste matters in the body, but a specific cure hasn’t been found as a lasting solution to AKI. In this study, ramipril was evaluated for its potential therapy in glycerol-induced AKI in rats. Methods Twenty animals were divided into four groups of five animals each. Group I was the control while group II was given glycerol on day 8 only, groups III and IV were administered with pioglitazone (reference drug) and ramipril for seven days respectively and on day 8 received glycerol. On the ninth day, blood and tissue samples were taken to assay for serum indicators of oxidative damage, enzymatic and nonenzymatic antioxidants, and creatinine and blood urea nitrogen. Animals were sacrificed thereafter; kidney was harvested for histological and immunohistochemical analysis. Expressions of caspase 3, renin receptor, NK-KB, and KIM-1 were carried out. Results Ramipril significantly inhibited indicators of oxidative damage while also significantly increasing levels of enzymatic and nonenzymatic antioxidant markers. These drugs also significantly lowered the levels of creatinine and blood urea nitrogen. Histology also indicated that while there were massive infiltration of leucocytes and congestion of the kidney in toxicant group, the ramipril-treated group showed a milder condition. In immunohistochemistry, the two drugs significantly inhibited the expressions of the four proteins, which were highly expressed in the toxicant group. Conclusions The study showed that ramipril and pioglitazone have nephroprotective effect and thus have the ability to blunt AKI through their anti-inflammatory, antiapoptosis, antirenin, and antioxidant properties.
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- 2020
9. Luteolin‐mediated Kim‐1/NF‐kB/Nrf2 signaling pathways protects sodium fluoride‐induced hypertension and cardiovascular complications
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Olufunke Olubunmi Falayi, Momoh A. Yakubu, Olumuyiwa Abiola Adejumobi, Adebowale Bernard Saba, Jeremiah Moyinoluwa Afolabi, Adeolu Alex Adedapo, Temidayo Olutayo Omobowale, Ebunoluwa Racheal Asenuga, Temitayo Olabisi Ajibade, Blessing Seun Ogunpolu, Olufunke Eunice Ola-Davies, and Ademola Adetokunbo Oyagbemi
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Glycation End Products, Advanced ,Male ,0301 basic medicine ,Mean arterial pressure ,Clinical Biochemistry ,Glutathione reductase ,Blood Pressure ,Pharmacology ,Kidney ,Nitric Oxide ,medicine.disease_cause ,Biochemistry ,Drug Administration Schedule ,Protein Carbonylation ,Electrocardiography ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Malondialdehyde ,Sodium fluoride ,medicine ,Animals ,Rats, Wistar ,Luteolin ,Antihypertensive Agents ,chemistry.chemical_classification ,Glutathione Peroxidase ,Superoxide Dismutase ,Glutathione peroxidase ,Troponin I ,Heart ,General Medicine ,Glutathione ,Catalase ,Rats ,Oxidative Stress ,Glutathione Reductase ,030104 developmental biology ,Gene Expression Regulation ,chemistry ,030220 oncology & carcinogenesis ,Hypertension ,Sodium Fluoride ,Molecular Medicine ,Oxidative stress - Abstract
The use of sodium fluoride (NaF) as a major ingredient for tooth paste, 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 coadministered 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 bet (NF-κB), nuclear factor erythroid 2-related factors 2 (Nrf2), and cardiac troponin I (CTnI). Together, Luteolin coadministration 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. © 2018 BioFactors, 44(6):518-531, 2018.
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- 2018
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10. Quercetin attenuates hypertension induced by sodium fluoride via reduction in oxidative stress and modulation of HSP 70/ERK/PPARγ signaling pathways
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Oluwatosin Adetola Arojojoye, Olufunke Eunice Ola-Davies, Temitayo Olabisi Ajibade, Temidayo Olutayo Omobowale, Momoh A. Yakubu, Olumuyiwa Abiola Adejumobi, Fasilat Oluwakemi Hassan, Olufunke Olubunmi Falayi, Ebunoluwa Racheal Asenuga, Adeolu Alex Adedapo, Jeremiah Moyinoluwa Afolabi, Grace Onyeche Ochigbo, Blessing Seun Ogunpolu, Adebowale Benard Saba, and Ademola Adetokunbo Oyagbemi
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0301 basic medicine ,medicine.medical_specialty ,Antioxidant ,medicine.medical_treatment ,Clinical Biochemistry ,Diastole ,medicine.disease_cause ,Biochemistry ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Internal medicine ,Sodium fluoride ,medicine ,Kidney ,General Medicine ,body regions ,030104 developmental biology ,Endocrinology ,medicine.anatomical_structure ,Blood pressure ,chemistry ,030220 oncology & carcinogenesis ,Molecular Medicine ,Quercetin ,Fluoride ,Oxidative stress - Abstract
Hypertension is one of the silent killers in the world with high mortality and morbidity. The exposure of humans and animals to fluoride and/or fluoride containing compounds is almost inevitable. This study investigated the modulatory effects of quercetin on sodium fluoride (NaF)-induced hypertension and cardiovascular complications. Forty male rats were randomly separated into four groups (n =10). Group A animals served as the control, rats in Group B were exposed to 300 ppm of NaF, Groups C and D animals were exposed to 300 ppm of NaF along with quercetin orally at 50 mg/kg and 100 mg/kg orally by gavage, while NaF was administered in drinking water, respectively, for a week. Administration of NaF caused severe hypertension as indicated with significant increases in the systolic, diastolic, and mean arterial blood pressure, together with prolonged ventricular depolarization (QRS) and the time between the start of the Q wave and the end of the T wave in the heart's electrical cycle (QT) intervals when compared with controls. NaF significantly decreased the activities of antioxidant enzymes, caused increase in markers of oxidative stress and renal damage when compared with controls. Immunohistochemical staining revealed lower expressions of Hsp70, ERK, and PPARγ in the heart, kidney, and aorta of rats-administered NaF relative to the controls. Together, quercetin co-treatment with NaF restored blood pressure, normalized QRS interval, and improved antioxidant defense system. © 2018 BioFactors, 44(5):465-479, 2018.
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- 2018
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11. Amelioration of N ω ‐Nitro‐L‐Arginine Methyl Ester (L‐NAME)‐induced hypertension and cardio‐renal oxidative stress by the methanol bark extract of Persea americana
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Ademola Adetokunbo Oyagbemi, Rahamon Adedokun, Momoh A. Yakubu, Olumuyiwa Abiola Adejumobi, Adeolu Alex Adedapo, Blessing Seun Ogunpolu, and Temidayo Olutayo Omobowale
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Persea ,biology ,Chemistry ,biology.organism_classification ,medicine.disease_cause ,Biochemistry ,Medicinal chemistry ,chemistry.chemical_compound ,visual_art ,Genetics ,visual_art.visual_art_medium ,medicine ,Nitro ,Arginine methyl ester ,Bark ,Methanol ,Molecular Biology ,Oxidative stress ,Biotechnology - Published
- 2019
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12. Cobalt chloride toxicity elicited hypertension and cardiac complication via induction of oxidative stress and upregulation of COX-2/Bax signaling pathway
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Temitayo Olabisi Ajibade, Momoh A. Yakubu, Olumuyiwa Abiola Adejumobi, U J Okotie, Ebunoluwa Rachael Asenuga, O V Awoyomi, Fasilat Oluwakemi Hassan, Ademola Adetokunbo Oyagbemi, Olufunke Eunice Ola-Davies, Adeolu Alex Adedapo, Adebowale Benard Saba, Blessing Seun Ogunpolu, Temidayo Olutayo Omobowale, and Olufunke Olubunmi Falayi
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0301 basic medicine ,Male ,medicine.medical_specialty ,Health, Toxicology and Mutagenesis ,Inflammation ,Toxicology ,medicine.disease_cause ,Kidney ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Internal medicine ,medicine ,Animals ,Rats, Wistar ,bcl-2-Associated X Protein ,chemistry.chemical_classification ,030102 biochemistry & molecular biology ,biology ,business.industry ,Glutathione peroxidase ,Myocardium ,Heart ,General Medicine ,Glutathione ,Cobalt ,Up-Regulation ,Oxidative Stress ,medicine.anatomical_structure ,Blood pressure ,Endocrinology ,chemistry ,Catalase ,Cyclooxygenase 2 ,030220 oncology & carcinogenesis ,Toxicity ,Hypertension ,biology.protein ,medicine.symptom ,business ,Oxidative stress - Abstract
Cobalt is a ferromagnetic metal with extensive industrial and biological applications. To assess the toxic effects of, and mechanisms involved in cobalt chloride (CoCl2)-induced cardio-renal dysfunctions. Male Wistar rats were exposed orally, daily through drinking water to 0 ppm (control), 150 ppm, 300 ppm, and 600 ppm of CoCl2, respectively. Following exposure, results revealed significant ( p < 0.05) rise in markers of oxidative stress, but decreased activities of catalase, glutathione peroxidase, glutathione-S-transferase, and reduced glutathione content in cardiac and renal tissues. There were significant increases in systolic, diastolic, and mean arterial blood pressure at the 300- and 600-ppm level of CoCl2-exposed rats relative to the control. Prolongation of QT and QTc intervals was observed in CoCl2alone treated rats. Also, there were significant increases in the heart rates, and reduction in P wave, and PR duration of rats administered CoCl2. Histopathology of the kidney revealed peritubular and periglomerular inflammation, focal glomerular necrosis following CoCl2exposure. Further, cyclooxygenase-2 and B-cell associated protein X expressions were upregulated in the cardiac and renal tissues of CoCl2-exposed rats relative to the control. Combining all, results from this study implicated oxidative stress, inflammation, and apoptosis as pathologic mechanisms in CoCl2-induced hypertension and cardiovascular complications of rats.
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- 2019
13. Sodium fluoride induces hypertension and cardiac complications through generation of reactive oxygen species and activation of nuclear factor kappa beta
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Temitope Moses Ige, Adeolu Alex Adedapo, Momoh A. Yakubu, Temitayo Olabisi Ajibade, Ebunoluwa Racheal Asenuga, Temidayo Olutayo Omobowale, Blessing Seun Ogunpolu, Ademola Adetokunbo Oyagbemi, and Abiola Olumuyiwa Adejumobi
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0301 basic medicine ,medicine.medical_specialty ,Mean arterial pressure ,Health, Toxicology and Mutagenesis ,010501 environmental sciences ,Management, Monitoring, Policy and Law ,Toxicology ,medicine.disease_cause ,01 natural sciences ,03 medical and health sciences ,chemistry.chemical_compound ,Fluoride toxicity ,Internal medicine ,Sodium fluoride ,medicine ,0105 earth and related environmental sciences ,Kidney ,Creatinine ,General Medicine ,Malondialdehyde ,030104 developmental biology ,Blood pressure ,Endocrinology ,medicine.anatomical_structure ,chemistry ,Oxidative stress - Abstract
Human exposure to sodium fluoride through its daily usage is almost inevitable. Cardiovascular and renal dysfunction has been associated with fluoride toxicity. Therefore, this study investigated the mechanism of action of sodium fluoride (NaF) induced hypertension and cardiovascular complications Forty male albino rats of an average of 10 rats per group were used. Group A received clean tap water. Toxicity was induced in Group B to D by administering graded doses of NaF through drinking water ad libitum for 10 days at 150 ppm, 300 ppm, and 600 ppm concentration respectively. Following administration of NaF, there was significant increase in systolic pressure, diastolic pressure and mean arterial pressure. Markers of oxidative stress; malondialdehyde, hydrogen peroxide, advance oxidation protein products, and protein carbonyl were significantly increased in dose-dependent pattern in the cardiac and renal tissues of rats together with significant decrease in the GST activity in NaF-treated rats compared to the control. Also serum markers of inflammation, cardiac, and renal damage including myeloperoxidase, xanthine oxidase, blood urea nitrogen, creatinine, Lactate dehydrogenase (LDH), and Creatinine kinase myocardial band (CK-MB) significantly increased indicating induction of oxidative stress, renal, and cardiac damage after exposure. Histopathology of the kidney and heart revealed aberrations in the histological architecture in NaF-treated rats. Also, immunohistochemistry showed higher expression of nuclear factor kappa beta (NF-kB) in the cardiac and renal tissues of rats administered NaF. Combining all, these results indicate NaF-induced hypertension through generation of reactive oxygen species and activation of renal and cardiac NF-kB expressions. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1089-1101, 2017.
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- 2016
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14. Methanol stem extract of Moringa oleifera mitigates glycerol-induced acute kidney damage in rats through modulation of KIM-1 and NF-kB signaling pathways
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Oluwafemi Omoniyi Oguntibeju, Blessing Seun Ogunpolu, Adeolu Alex Adedapo, Ademola Adetokunbo Oyagbemi, Temidayo Olutayo Omobowale, Utibe Etim, and Olufunke Olubunmi Falayi
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Glycerol ,Pharmacology ,medicine.disease_cause ,Moringa ,Superoxide dismutase ,chemistry.chemical_compound ,Oxidative damage ,medicine ,NF-kB ,KIM-1 ,lcsh:Science ,Blood urea nitrogen ,Kidney ,Multidisciplinary ,biology ,Chemistry ,Acute kidney injury ,Glutathione ,medicine.disease ,Malondialdehyde ,medicine.anatomical_structure ,biology.protein ,lcsh:Q ,Oxidative stress - Abstract
Moringa oleifera popularly referred to as wonder plant is a medicinal plant with a remarkable variety of therapeutic purposes. The aim of this study was to assess the ameliorative effect of Moringa oleifera on glycerol-induced acute kidney injury in rats thus renewing interest in the development of new treatment plans. Glycerol (50% v/v in sterile saline, intramuscular) was used to induce acute kidney injury. Group A (control group) received distilled water only, the group B animals (toxicant group) received glycerol alone on the 8th day, and groups C and D animals were given 50 mg/kg and 100 mg/kg of methanol stem extract of Moringa oleifera respectively for seven days and glycerol on the 8th day. Group E animals on the other hand received 100 mg/kg of methanol stem extract of Moringa oleifera alone for seven days and on day 8 received normal saline. To assess renal damage and possible ameliorative effects of the extract, serum blood urea nitrogen (BUN), creatinine, myeloperoxidase, advanced oxidative products, malondialdehyde, superoxide dismutase, reduced glutathione, and protein carbonyl were determined. Histopathological analysis of kidney tissues and immunohistochemical analysis of KIM-1 and NF-ҝB expressions were also carried out on kidney tissues. The results showed that methanol stem bark extract of Moringa oleifera improves glycerol-induced acute kidney injury by inhibiting markers of inflammation, oxidative stress and renal damage by modulating KIM-1 and NF-ҝB signaling pathways. In conclusion, the methanol stem extract of Moringa oleifera blunts glycerol-induced acute kidney injury in rats through its anti-oxidant and anti-inflammatory properties.
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- 2020
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15. Antihypertensive power of Naringenin is mediated via attenuation of mineralocorticoid receptor (MCR)/ angiotensin converting enzyme (ACE)/ kidney injury molecule (Kim-1) signaling pathway
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Iyanuoluwa Omolola Ogunmiluyi, Oluwafemi Omoniyi Oguntibeju, Sanah M. Nkadimeng, Blessing Seun Ogunpolu, Ademola Adetokunbo Oyagbemi, Fasilat Oluwakemi Hassan, Olufunke Eunice Ola-Davies, Momoh A. Yakubu, Olumuyiwa Abiola Adejumobi, Adebowale Benard Saba, K. O. Soetan, Abiodun Mary Owolabi, Adeolu Alex Adedapo, Olufunke Olubunmi Falayi, Ebunoluwa Racheal Asenuga, Lyndy Joy McGaw, and Temidayo Olutayo Omobowale
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Male ,0301 basic medicine ,Naringenin ,medicine.medical_specialty ,Peptidyl-Dipeptidase A ,Kidney ,Nitric oxide ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Mineralocorticoid receptor ,Internal medicine ,medicine ,Animals ,Rats, Wistar ,Blood urea nitrogen ,Antihypertensive Agents ,Neurons ,Pharmacology ,Creatinine ,biology ,Chemistry ,Lisinopril ,Brain ,Angiotensin-converting enzyme ,Oxidative Stress ,NG-Nitroarginine Methyl Ester ,Receptors, Mineralocorticoid ,030104 developmental biology ,Endocrinology ,Blood pressure ,Flavanones ,Hypertension ,biology.protein ,Cell Adhesion Molecules ,030217 neurology & neurosurgery ,Signal Transduction ,medicine.drug - Abstract
Hypertension is a condition with chronic elevation of blood pressure and a common preventable risk factor for cardiovascular disease with attendant global morbidity and mortality. The present study investigated the novel antihypertensive and neuroprotective effect of Naringenin on L-NG-Nitro arginine methyl ester (L-NAME) induced hypertension together with possible molecular mechanism of action. Rats were divided into four groups. Rats in Group A were normotensive. The hypertensive group (Group B) received 40 mg/kg) of L-NAME alone while Groups C and D were concurrently administered Naringenin (50 mg/kg) or Lisinopril (10 mg/Kg) together with L-NAME orally for 3 weeks. Blood pressure parameters, markers of oxidative stress and renal damage were measured. The immunohistochemistry of kidney injury molecule 1, mineralocorticoid receptor and angiotensin converting enzyme were also determined. Results indicated significant increases in malondialdehyde, advanced oxidation protein products, protein carbonyl contents and decrease in serum nitric oxide bioavailability in hypertensive rats. Furthermore, there were significant increases in serum myeloperoxidase, urinary creatinine, albumin and blood urea nitrogen in hypertensive rats in comparison to hypertensive rats treated with either Naringenin or Lisinopril. Immunohistochemistry reveal significant expressions of kidney injury molecule 1, mineralocorticoid receptor and angiotensin converting enzyme in hypertensive rats. However, co-treatment with either Naringenin or Lisinopril mitigated both renal and neuronal oxidative stress, normalized blood pressure and lowered the expressions of kidney injury molecule 1, mineralocorticoid receptor and angiotensin converting enzyme. Collectively, Naringenin offered a novel antihypertensive and neuroprotective effect through down regulation of kidney injury molecule 1, mineralocorticoid receptor and angiotensin converting enzyme.
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- 2020
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16. Influence of Oxidative stress and NF‐κβ/CRP/Bcl‐2 Signaling on Gentamicin Induced Renal Toxicology and the ameliorative effect of chloroform extract of Abrus precatorius in male Wistar rats
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Adeolu Alex Adedapo, Olufunke Olubunmi Falayi, Temidayo Olutayo Omobowale, Blessing Seun Ogunpolu, Momoh A. Yakubu, and Ademola Adetokunbo Oyagbemi
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Chloroform ,biology ,Pharmacology ,medicine.disease_cause ,biology.organism_classification ,Biochemistry ,chemistry.chemical_compound ,chemistry ,Abrus precatorius ,Genetics ,medicine ,Gentamicin ,Molecular Biology ,Oxidative stress ,Biotechnology ,medicine.drug - Published
- 2020
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17. Antihypertensive effect of methanol leaf extract of Azadirachta indica is mediated through suppression of renal caspase 3 expressions on Nω-Nitro-l-arginine methyl ester induced hypertension
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Idayat Titilayo Gbadamos, Oluwafemi Omoniyi Oguntibeju, Adebowale Bernard Saba, Temidayo Olutayo Omobowale, Adeolu Alex Adedapo, Ebunoluwa Racheal Asenuga, Anofi Ashafa, Blessing Seun Ogunpolu, Momoh A. Yakubu, Olumuyiwa Abiola Adejumobi, Olufunke Olubunmi Falayi, Temitayo Olabisi Ajibade, Olufunke Eunice Ola-Davies, Jeremiah Moyinoluwa Afolabi, Fisayo Olutayo Ugbor, and Ademola Adetokunbo Oyagbemi
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Pharmacology ,Meliaceae ,Antioxidant ,biology ,Chemistry ,medicine.medical_treatment ,Azadirachta ,biology.organism_classification ,medicine.disease_cause ,law.invention ,Blood pressure ,law ,Drug Discovery ,medicine ,Arterial blood ,Enalapril ,Phytotherapy ,Oxidative stress ,medicine.drug - Abstract
Background: Azadirachta indica (AI) Adr Juss (Meliaceae), known as neem, has been used traditionally for the treatment of various disease conditions including obesity and hypertension. Objective: The antihypertensive effect and mechanism of action of modulatory effect of AI were investigated after the induction of hypertension using Nω-nitro-L-arginine methyl ester (L-NAME). Materials and Methods: Five groups of ten rats divided as follows: Control; L-NAME (40 mg/kg); L-NAME + 100 mg/kg AI; L-NAME and 200 mg/kg ?AI; and L-NAME and Enalapril (25 mg/kg) were used. Results: following the application of L-NAME, hypertension (elevated systolic, diastolic, mean arterial blood pressures) and increased levels of oxidative stress markers were observed in rats. Immunohistochemistry showed increased caspase-3 expressions in hypertensive rats compared to normotensive rats. Conversely, AI treatment resulted in restoration of physiological antioxidant status and normotension, comparable to the standard antihypertensive agent enalapril. Conclusion: AI leaf is a good candidate for the management of high blood pressure.
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- 2020
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18. Antihypertensive Effect of Polyphenol-Rich Fraction of Azadirachta indica on Nω-Nitro-L-Arginine Methyl Ester-Induced Hypertension and Cardiorenal Dysfunction
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J. O. Olukunle, Temidayo Olutayo Omobowale, Ademola Adetokunbo Oyagbemi, Jeremiah Moyinoluwa Afolabi, Momoh A. Yakubu, Olumuyiwa Abiola Adejumobi, Blessing Seun Ogunpolu, Anofi Omotayo Tom Ashafa, Adeolu Alex Adedapo, Ebunoluwa Racheal Asenuga, Olufunke Olubunmi Falayi, Temitayo Olabisi Ajibade, and Olufunke Eunice Ola-Davies
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0301 basic medicine ,chemistry.chemical_classification ,Antioxidant ,biology ,Glutathione peroxidase ,medicine.medical_treatment ,Captopril ,General Medicine ,Pharmacology ,Azadirachta ,medicine.disease_cause ,biology.organism_classification ,Malondialdehyde ,Nitric oxide ,03 medical and health sciences ,chemistry.chemical_compound ,030104 developmental biology ,Blood pressure ,chemistry ,Drug Discovery ,medicine ,Oxidative stress ,medicine.drug - Abstract
Azadirachta indica (AI) is a medicinal plant with reported antioxidant 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 Nω-Nitro-L-Arginine Methyl Ester (L-NAME) 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 AI extract, 40 mg/kg of L-NAME and 200 mg/kg of AI 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 AI restored high blood pressure, reduced markers of oxidative stress, normalized serum NO bioavailability and increased the expressions of Nrf2. Hence, PRF of Azadirachta indica could be used for the treatment of hypertension.
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- 2018
19. Quercetin attenuates hypertension induced by sodium fluoride via reduction in oxidative stress and modulation of HSP 70/ERK/PPARγ signaling pathways
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Ademola Adetokunbo, Oyagbemi, Temidayo Olutayo, Omobowale, Olufunke Eunice, Ola-Davies, Ebunoluwa Racheal, Asenuga, Temitayo Olabisi, Ajibade, Olumuyiwa Abiola, Adejumobi, Oluwatosin Adetola, Arojojoye, Jeremiah Moyinoluwa, Afolabi, Blessing Seun, Ogunpolu, Olufunke Olubunmi, Falayi, Fasilat Oluwakemi, Hassan, Grace Onyeche, Ochigbo, Adebowale Benard, Saba, Adeolu Alex, Adedapo, and Momoh Audu, Yakubu
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MAP Kinase Signaling System ,Superoxide Dismutase ,Blood Pressure ,Glutathione ,Antioxidants ,Rats ,PPAR gamma ,Oxidative Stress ,Hypertension ,Animals ,Humans ,Sodium Fluoride ,HSP70 Heat-Shock Proteins ,Quercetin ,Lipid Peroxidation ,Rats, Wistar ,Signal Transduction - Abstract
Hypertension is one of the silent killers in the world with high mortality and morbidity. The exposure of humans and animals to fluoride and/or fluoride containing compounds is almost inevitable. This study investigated the modulatory effects of quercetin on sodium fluoride (NaF)-induced hypertension and cardiovascular complications. Forty male rats were randomly separated into four groups (n =10). Group A animals served as the control, rats in Group B were exposed to 300 ppm of NaF, Groups C and D animals were exposed to 300 ppm of NaF along with quercetin orally at 50 mg/kg and 100 mg/kg orally by gavage, while NaF was administered in drinking water, respectively, for a week. Administration of NaF caused severe hypertension as indicated with significant increases in the systolic, diastolic, and mean arterial blood pressure, together with prolonged ventricular depolarization (QRS) and the time between the start of the Q wave and the end of the T wave in the heart's electrical cycle (QT) intervals when compared with controls. NaF significantly decreased the activities of antioxidant enzymes, caused increase in markers of oxidative stress and renal damage when compared with controls. Immunohistochemical staining revealed lower expressions of Hsp70, ERK, and PPARγ in the heart, kidney, and aorta of rats-administered NaF relative to the controls. Together, quercetin co-treatment with NaF restored blood pressure, normalized QRS interval, and improved antioxidant defense system. © 2018 BioFactors, 44(5):465-479, 2018.
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- 2018
20. Ameliorative effect of Rutin on sodium fluoride-induced hypertension through modulation of Kim-1/NF-κB/Nrf2 signaling pathway in rats
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Ebunoluwa Racheal Asenuga, Temitayo Olabisi Ajibade, Adebowale Bernard Saba, Momoh A. Yakubu, Olumuyiwa Abiola Adejumobi, Ademola Adetokunbo Oyagbemi, Adeolu Alex Adedapo, Olufunke Eunice Ola-Davies, Blessing Seun Ogunpolu, Olufunke Olubunmi Falayi, Jeremiah Moyinoluwa Afolabi, Fasilat Oluwakemi Hassan, Fatimah Ayodeji, and Temidayo Olutayo Omobowale
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0301 basic medicine ,Male ,Antioxidant ,NF-E2-Related Factor 2 ,Health, Toxicology and Mutagenesis ,medicine.medical_treatment ,Rutin ,Blood Pressure ,Management, Monitoring, Policy and Law ,Pharmacology ,Toxicology ,medicine.disease_cause ,Antioxidants ,Nitric oxide ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Sodium fluoride ,medicine ,Animals ,Rats, Wistar ,Saline ,Chemistry ,NF-kappa B ,General Medicine ,Bioavailability ,Rats ,Oxidative Stress ,030104 developmental biology ,Blood pressure ,030220 oncology & carcinogenesis ,Hypertension ,Sodium Fluoride ,Cell Adhesion Molecules ,Oxidative stress ,Signal Transduction - Abstract
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 NaF in drinking water, while Groups C and D received NaF along Rutin (100 mg/kg and 200 mg/kg) orally daily for a week. Administration of NaF alone led to significant increases in blood pressure, and deceased serum nitric oxide. Immunohistochemistry revealed higher expressions of kidney injury molecule I (Kim-1), nuclear factor kappa beta (NF-κB), and down regulation of nuclear factor erythroid 2-related factor 2 (Nrf2) in rats administered NaF. Rutin co-treatment with NaF normalized blood pressure, lowered Kim-1 and NF-κB expressions, and improved nitric oxide bioavailability.
- Published
- 2018
21. Lack of reversal of oxidative damage in renal tissues of lead acetate-treated rats
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Ademola Adetokunbo Oyagbemi, Adebowale Bernard Saba, Blessing Seun Ogunpolu, Akinleye Stephen Akinrinde, Temidayo Olutayo Omobowale, and Oluwabusola Daramola
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medicine.medical_specialty ,biology ,Chemistry ,Health, Toxicology and Mutagenesis ,General Medicine ,Glutathione ,Management, Monitoring, Policy and Law ,Toxicology ,Malondialdehyde ,medicine.disease_cause ,Nephrotoxicity ,Superoxide dismutase ,chemistry.chemical_compound ,Endocrinology ,Biochemistry ,Catalase ,Lead acetate ,Internal medicine ,biology.protein ,medicine ,Blood urea nitrogen ,Oxidative stress - Abstract
Removal of lead from the environment of man or otherwise, the movement of man from lead-contaminated areas has been employed as a means of abatement of the toxic effects of lead. Whether toxic effects in already-exposed individuals subside after lead withdrawal remains unanswered. To understand the reversibility of nephrotoxicity induced by lead acetate, male Wistar rats were orally exposed to 0.25, 0.5, and 1.0 mg/mL of lead acetate for 6 weeks. Activities of glutathione-s-transferase, catalase (CAT), superoxide dismutase (SOD) and the concentrations of hydrogen peroxide (H2O2), and malondialdehyde increased significantly (p
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- 2014
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22. Cobalt chloride exposure dose-dependently induced hepatotoxicity through enhancement of cyclooxygenase-2 (COX-2)/B-cell associated protein X (BAX) signaling and genotoxicity in Wistar rats
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Ademola Adetokunbo Oyagbemi, Ufuoma Jowafe Okotie, Ebunoluwa Racheal Asenuga, Temidayo Olutayo Omobowale, Blessing Seun Ogunpolu, Omolola Victoria Awoyemi, and Olufunke Eunice Ola-Davies
- Subjects
0301 basic medicine ,Male ,Antioxidant ,Erythroblasts ,Health, Toxicology and Mutagenesis ,medicine.medical_treatment ,Inflammation ,Apoptosis ,010501 environmental sciences ,Management, Monitoring, Policy and Law ,Pharmacology ,Toxicology ,medicine.disease_cause ,01 natural sciences ,Antioxidants ,03 medical and health sciences ,medicine ,Animals ,Rats, Wistar ,0105 earth and related environmental sciences ,bcl-2-Associated X Protein ,chemistry.chemical_classification ,biology ,General Medicine ,Cobalt ,Oxidative Stress ,030104 developmental biology ,Enzyme ,chemistry ,Cyclooxygenase 2 ,Micronucleus test ,biology.protein ,Environmental Pollutants ,Cyclooxygenase ,medicine.symptom ,Chemical and Drug Induced Liver Injury ,Genotoxicity ,Oxidative stress ,DNA Damage ,Mutagens ,Signal Transduction - Abstract
Cobalt chloride (CoCl2 ) is one of the many environmental contaminants, used in numerous industrial sectors. It is a pollutant with deadly toxicological consequences both in developing and developed countries. We investigated toxicological impact of CoCl2 on hepatic antioxidant status, apoptosis, and genotoxicity. Forty Wistar rats were divided into four groups, 10 rats per group: Group 1 served as control and received clean tap water orally; Group 2 received CoCl2 solution (150 mg/L); Group 3 received CoCl2 solution (300 mg/L); and Group 4 received CoCl2 (600 mg/L) in drinking water for 7 days, respectively. Exposure of rats to CoCl2 led to a significant decline in hepatic antioxidant enzymes together with significant increase in markers of oxidative stress. Immunohistochemistry revealed dose-dependent increase in cyclooxygenase-2 and BAX expressions together with increased frequency of Micronucleated Polychromatic Erythrocytes. Combining all, CoCl2 administration led to hepatic damage through induction of oxidative stress, inflammation, and apoptosis.
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- 2016
23. Sodium fluoride induces hypertension and cardiac complications through generation of reactive oxygen species and activation of nuclear factor kappa beta
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Ademola Adetokunbo, Oyagbemi, Temidayo Olutayo, Omobowale, Ebunoluwa Racheal, Asenuga, Abiola Olumuyiwa, Adejumobi, Temitayo Olabisi, Ajibade, Temitope Moses, Ige, Blessing Seun, Ogunpolu, Adeolu Alex, Adedapo, and Momoh Audu, Yakubu
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Male ,Myocardium ,NF-kappa B ,Kidney ,Cariostatic Agents ,Rats ,Oxidative Stress ,Malondialdehyde ,Hypertension ,Animals ,Sodium Fluoride ,Rats, Wistar ,Reactive Oxygen Species ,Biomarkers - Abstract
Human exposure to sodium fluoride through its daily usage is almost inevitable. Cardiovascular and renal dysfunction has been associated with fluoride toxicity. Therefore, this study investigated the mechanism of action of sodium fluoride (NaF) induced hypertension and cardiovascular complications Forty male albino rats of an average of 10 rats per group were used. Group A received clean tap water. Toxicity was induced in Group B to D by administering graded doses of NaF through drinking water ad libitum for 10 days at 150 ppm, 300 ppm, and 600 ppm concentration respectively. Following administration of NaF, there was significant increase in systolic pressure, diastolic pressure and mean arterial pressure. Markers of oxidative stress; malondialdehyde, hydrogen peroxide, advance oxidation protein products, and protein carbonyl were significantly increased in dose-dependent pattern in the cardiac and renal tissues of rats together with significant decrease in the GST activity in NaF-treated rats compared to the control. Also serum markers of inflammation, cardiac, and renal damage including myeloperoxidase, xanthine oxidase, blood urea nitrogen, creatinine, Lactate dehydrogenase (LDH), and Creatinine kinase myocardial band (CK-MB) significantly increased indicating induction of oxidative stress, renal, and cardiac damage after exposure. Histopathology of the kidney and heart revealed aberrations in the histological architecture in NaF-treated rats. Also, immunohistochemistry showed higher expression of nuclear factor kappa beta (NF-kB) in the cardiac and renal tissues of rats administered NaF. Combining all, these results indicate NaF-induced hypertension through generation of reactive oxygen species and activation of renal and cardiac NF-kB expressions. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1089-1101, 2017.
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- 2016
24. Failure of recovery from lead‐acetate‐induced oxidative stress and cardiotoxicity in Wistar rats (648.14)
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Temidayo Olutayo Omobowale, Blessing Seun Ogunpolu, Oyagbemi Ademola, Temilade Daramola, Adebowale Bernard Saba, and Stephen Akinrinde
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Cardiotoxicity ,Lead acetate ,Chemistry ,Genetics ,medicine ,Pharmacology ,medicine.disease_cause ,Molecular Biology ,Biochemistry ,Oxidative stress ,Biotechnology - Published
- 2014
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25. Lack of reversal from lead acetate‐induced hepatotoxicity, free radical generation and oxidative stress in Wistar rats (1139.17)
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Blessing Seun Ogunpolu, Oluwabusola Daramola, Ademola Adetokunbo Oyagbemi, Adebowale Bernard Saba, Temidayo Olutayo Omobowale, and Akinleye Stephen Akinrinde
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Chemistry ,Lead acetate ,Genetics ,medicine ,Pharmacology ,medicine.disease_cause ,Molecular Biology ,Biochemistry ,Oxidative stress ,Biotechnology - Published
- 2014
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26. Failure of recovery from lead induced hepatoxicity and disruption of erythrocyte antioxidant defence system in Wistar rats
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Akinleye Stephen Akinrinde, Ademola Adetokunbo Oyagbemi, Adebowale Bernard Saba, Oluwabusola Daramola, Temidayo Olutayo Omobowale, Blessing Seun Ogunpolu, and James O. Olopade
- Subjects
Male ,medicine.medical_specialty ,Antioxidant ,Erythrocytes ,Health, Toxicology and Mutagenesis ,medicine.medical_treatment ,Toxicology ,medicine.disease_cause ,Superoxide dismutase ,chemistry.chemical_compound ,Internal medicine ,parasitic diseases ,medicine ,Organometallic Compounds ,Animals ,Aspartate Aminotransferases ,Rats, Wistar ,Glutathione Transferase ,Pharmacology ,chemistry.chemical_classification ,Glutathione Peroxidase ,biology ,Superoxide Dismutase ,Glutathione peroxidase ,Alanine Transaminase ,General Medicine ,Glutathione ,Malondialdehyde ,Catalase ,Endocrinology ,chemistry ,Biochemistry ,Hematocrit ,Liver ,Lead acetate ,Cyclooxygenase 2 ,biology.protein ,Environmental Pollutants ,Chemical and Drug Induced Liver Injury ,Oxidative stress - Abstract
Lead acetate (PbA) is one of the major environmental contaminants with grave toxicological consequences both in the developing and developed countries. The liver and erythrocyte antioxidant status and markers of oxidative were assessed. Exposure of rats to PbA led to significant decline (p < 0.05) in hepatic and erythrocyte glutathione peroxidase (GPx), glutathione S-transferase (GST), catalase (CAT), superoxide dismutase (SOD), and reduced glutathione (GSH) content. Similarly, malondialdehyde (MDA) and H(2)O(2) concentrations were significantly (p < 0.05) elevated. Histopathology and immunohistology of liver of rats exposed to PbA showed focal areas of necrosis and COX-2 expression after 6 weeks of PbA withdrawal. Taken together, hepatic and erythrocytes antioxidant defence system failed to recover after withdrawal of the exposed PbA for the period of the study. In conclusion, experimental animals exposed to PbA did not recover from hepatotoxicity and disruption of erythrocyte antioxidant defence system via free radical generation and oxidative stress.
- Published
- 2013
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