Browsing by Author "Hassan, F. O."

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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
Antihypertensive Power of Naringenin is Mediated via Attenuation of Mineralocorticoid Receptor (MCR)/ Angiotensin Converting Enzyme (ACE)/ Kidney Injury Molecule (Kim-1) Signaling Pathway
(Elsevier B.V, 2020) Oyagbemi, A. A.; Omobowale, T. O.; Adejumobi, O. A.; Owolabi, A. M.; Ogunpolu, B. S.; Falayi, O. O.; Hassan, F. O.; Ogunmiluyi, I. O.; Asenuga, E. R.; Ola-Davies, O. E.; Soetan, K. O.; Saba, A. B.; Adedapo, A. A.; Nkadimeng, S. M.; McGaw, L. J.; Oguntibeju, O. O.; Yakubu, M. A.
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 revealed 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 downregulation of kidney injury molecule 1, mineralocorticoid receptor and angiotensin converting enzyme.
Clofibrate, a peroxisome proliferator-activated receptor-alpha (PPARα) agonist, and its molecular mechanisms of action against sodium fluoride-induced toxicity
(Springer Nature, 2021) Oyagbemi, A. A.; Adejumobi, O. A.; Jarikre, T. A.; Ajani, S. O.; Asenuga, E. R.; Gbadamosi, I. T.; Adedapo, A. D. A.; Aro, A. O.; Ogunpolu, B. S.; Hassan, F. O.; Falayi, O. O.; Ogunmiluyi, I. O.; Omobowale, T. O.; Arojojoye, O. A.; Ola-Davies, O. E.; Saba, A. B.; Adedapo, A. A.; Emikpe, B. O.; Oyeyemi, M. O.; Nkadimeng, S. M.; McGaw, L. J.; Kayoka-Kabongo, P. N.; Oguntibeju, O. O.; Yakubu, M. A.
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.
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
(Wiley, 2020) Oyagbemi, A. A.; Adebiyi, O. E.; Adigun, K. O.; Ogunpolu, B. S.; Falayi, O. O.; Hassan, F. O.; Folarin, O. R.; Adebayo, A. K.; Adejumobi, O. A.; Asenuga, E. R.; Ola-Davies, O. E.; Omobowale, T. O.; Olopade, J. O.; Saba, A. B.; Adedapo, A. A.; Nkadimeng, S. M.; McGaw, L. J.; Oguntibeju, O. O.; Yakubu, M. A.
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 neu- rotoxicity, and motor disorders. The neuroprotective effect of clofibrate, a peroxi some 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 1300 ppm), NaF plus clofi- brate (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, acetylcholin- esterase activity, and neurobehavioral thanging wire and open field) tests were per- formed. 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 sig nificantly 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. Neuro- behavioral results showed that cotreatment of NaF with clofibrate improved muscu lar strength and locomotion, reduced anxiety, and significantly reduced astrocytic count. Overall, cotreatment of Naf with either clofibrate or lisinopril showed neuro- protective effects by mitigating neuronal inflammation and oxidative and motor inco ordination. Hence, clofibrate could be seen as a novel drug candidate against neurodegeneration and motor disorders.
Cobalt Chloride Toxicity Elicited Hypertension and Cardiac Complication Via Induction of Oxidative Stress and Upregualtion of Cox-2/ Bax Signaling Pathway
(SAGE Publications Ltd, 2019) Oyagbemi, A. A.; Omobowale, T. O.; Awoyomi, O. V.; Ajibade, T. O.; Falayi, O. O.; Ogunpolu, B. S.; Okotie, U. J.; Asenuga, E. R.; Adejumobi, O. A.; Hassan, F. O.; Ola-Davies, O. E.; Saba, A. B.; Adedapo, A. A.; Yakubu, M. A.
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 Cobalt chloride, 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 Cobalt chloride-exposed rats relative to the control. Prolongation of QT and QTc intervals was observed in Cobalt chloride alone treated rats. Also, there were significant increases in the heart rates, and reduction in P wave, and PR duration of rats administered Cobalt chloride. Histopathology of the kidney revealed peritubular and periglomerular inflammation, focal glomerular necrosis following Cobalt chloride exposure. Further, cyclooxygenase-2 and B-cell associated protein X expressions were upregulated in the cardiac and renal tissues of Cobalt chloride-exposed rats relative to the control. Combining all, results from this study implicated oxidative stress, inflammation, and apoptosis as pathologic mechanisms in Cobalt chloride-induced hypertension and cardiovascular complications of rats.
Luteolin Attenuates Glycerol-Induced Acute Renal Failure and Cardiac Complications Through Modulation of Kim-1/NF-κB/Nrf2 Signaling Pathways
(Taylor & Francis, 2020) Oyagbemi, A. A.; Adejumobi, O. A.; Ajibade, T. O.; Asenuga, E. R.; Afolabi, J. M.; Ogunpolu, B. S.; Falayi, O. O.; Hassan, F. O.; Nabofa, E. W.; Omobowale, T. O.; Ola-Davies, O. E.; Saba, A. B.; Adedapo, A. A.; Oguntibeju, O. O.; Yakubu, M. A.
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 (n = 10). Group A received normal saline. Group B received glycerol (10 ml/kg BW, 50% v/v in sterile saline, i.m.). Groups C and D were pretreated with Luteolin 100 and 200 mg/kg for 7 days, and thereafter administered glycerol (10 ml/kg BW, 50% v/v in sterile saline, i.m.). Administration of glycerol significantly increased systolic blood pressure, diastolic blood pressure and mean arterial pressure. Renal protein carbonyl and xanthine oxidase increased significantly while significant reduction in the activity of renal glutathione peroxidase, glutathione S-transferase and glutathione reductase was observed in the glycerol intoxicated rats. Furthermore, administration of glycerol led to significant increases in serum creatinine and blood urea nitrogen together with reduction in nitric oxide (NO) bioavailability. Immunohistochemistry revealed that glycerol intoxication enhanced expressions of kidney injury molecule 1, nuclear factor kappa beta and cardiac troponin (CTnI). However, Luteolin pretreatment normalized blood pressure, reduced markers of oxidative stress and renal damage, and improved NO bioavailability. Luteolin also downregulated the expressions of kidney injury molecule 1, nuclear factor kappa beta and cardiac troponin. Together, Luteolin might open a novel therapeutic window for the treatment of acute renal failure and cardiac complications.
Potential health benefits of zinc supplementation for the management of the COVID-19 pandemic
(Wiley, 2020) Oyagbemi, A. A.; Ajibade, T. O.; Aboua, Y. G.; Gbadamosi, I. T.; Adedapo, A. D. A.; Aro, A. O.; Adejumobi, O. A.; Thamahane-Katengua, E.; Omobowale, T. O.; Falayi, O. O.; Oyagbemi, T. O.; Ogunpolu, B. S.; Hassan, F. O.; Ogunmiluyi, I. O.; Ola-Davies, O. E.; Saba, A. B.; Adedapo, A. A.; Nkadimeng, S. M.; McGaw, L. J.; Kayoka-Kabongo, P. N.; Oguntibeju, O. O.; Yakubu, M. A.
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiological agent for the Coronavirus Disease 2019 (COVID-19). The COVID-19 pandemic has created unimaginable and unprecedented global health crisis. Since the outbreak of COVID-19, millions of dollars have been spent, hospitalization overstretched with increasing morbidity and mortality. All these have resulted in unprecedented global economic catastrophe. Several drugs and vaccines are currently being evaluated, tested, and administered in the frantic efforts to stem the dire consequences of COVID-19 with varying degrees of successes. Zinc possesses potential health benefits against COVID-19 pandemic by improving immune response, minimizing infection and inflammation, preventing lung injury, inhibiting viral replication through the interference of the viral genome transcription, protein translation, attachment, and host infectivity. However, this review focuses on the various mechanisms of action of zinc and its supplementation as adjuvant for vaccines an effective therapeutic regimen in the management of the ravaging COVID-19 pandemic.
Quercetin Attenuates Hypertension Induced by Sodium Fluoride Via Reduction in Oxidative Stress and Modulation of HSP70/ERK/PPARγ Signaling Pathways
(Wiley-Blackwell, 2018) Oyagbemi, A. A.; Omobowale, T. O.; Ola-Davies, O. E.; Asenuga, E. R.; Ajibade, T. O.; Adejumobi, O. A.; Arojojoye, O. A.; Afolabi, J. M.; Ogunpolu, B. S.; Falayi, O. O.; Hassan, F. O.; Ochigbo, G. O.; Saba, A. B.; Adedapo, A. A.; Yakubu, M. A.
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 Sodium fluoride, Groups C and D animals were exposed to 300 ppm of Sodium fluoride along with Quercetin orally at 50 mg/kg and 100 mg/kg orally by gavage, while Sodium fluoride was administered in drinking water, respectively, for a week. Administration of Sodium fluoride caused severe hypertension as indicated by significant increases in systolic, diastolic, and mean arterial blood pressure, together with prolonged ventricular depolarization (QRS) and QT intervals when compared with controls. Sodium fluoride 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 Sodium fluoride relative to the controls. Together, Quercetin co-treatment with Sodium fluoride restored blood pressure, normalized QRS interval, and improved antioxidant defense system.
The therapeutic potential of the novel angiotensin-converting enzyme 2 in the treatment of coronavirus disease 2019 (COVID-19)
(Horizon Publisher India, 2021) Oyagbemi, O. A.; Ajibade, T. O.; Abowa, Y. G.; Gbadamosi, I. I.; Adedapo, A. D. A.; Aro, A. O.; Adejumobi, O. A.; Thamahane-Katenuga, E.; Omobowale, T. O.; Falayi, O. O.; Oyagbemi, T. O.; Ogunpolu, B. S.; Hassan, F. O.; Ogunmiluyi, I. O.; Ola-Davies, O. E.; Saba, A. B.; Adedapo, A. A.; Nkadimeng, S. M.; McGaw, L. Z.; Kayoka-Kabongo, P. N.; Yakubu, M. A.; Oguntibeju, O. O.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiological agent of coronavirus disease 2019 (COVID-19). This virus has become a global pandemic with unprecedented mortality and morbidity along with attendant financial and economic crises. Furthermore, COVID-19 can easily be transmitted regardless of religion, race, sex, or status. Globally, high hospitalization rates of COVID-19 patients have been reported, and billions of dollars have been spent to contain the pandemic. Angiotensin-converting enzyme (ACE) 2 is a receptor of SARS-CoV-2, which has a significant role in the entry of the virus into the host cell. ACE2 is highly expressed in the type II alveolar cells of the lungs, upper esophagus, stratified epithelial cells, and other tissues in the body. The diminished expressions of ACE2 have been associated with hypertension, arteriosclerosis, heart failure, chronic kidney disease, and immune system dysregulation. Overall, the potential drug candidates that could serve as ACE2 activators or enhance the expression of ACE2 in a disease state, such as COVID-19, hold considerable promise in mitigating the COVID-19 pandemic. This study reviews the therapeutic potential and pharmacological benefits of the novel ACE2 in the management of COVID-19 using search engines, such as Google, Scopus, PubMed, and PubMed Central.