Browsing by Author "Ogunpolu, B. S."

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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 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.
Antihypertensive effect of Methanol Leaf Extract of Azadirachta inidica is Mediated through Suppression of Renal Caspase 3 Expression on Nω-Nitro-L-Arginine Methyl Ester. Pharmacognosy
(Phcog.Net, 2020) Omobowale, T. O.; Oyagbemi, A. A.; Adejumobi, O. A.; Ugbor, F.; Asenuga, E. R.; Ajibade, T. O.; Afolabi, J. M.; Ogunpolu, B. S.; Falayi, O. O.; Gbadamosi, F. T.; Ola-Davies, O. E.; Saba, A. B.; Ashafa, A.; Yakubu, M. A.; Adedapo, A. A.; Oguntibeju, O. O.
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.
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 exposure dose dependently induced hepatotoxicity through enhancement of cyclooxygenase-2 (COX-2)/B- cell associated protein X (BAX) signaling and genotoxicity in wistar rats
(Wiley, 2017-02) Awoyemi, O. V.; Okotie, U. J.; Oyagbemi, A. A.; Omobowale, T. O.; Asenuga, E. R.; Ola-Davies, O. E.; Ogunpolu, B. S.
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.
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.
Failure of recovery from lead induced hepatotoxicity and disruption of erythrocyte antioxidant defense system in Wistar rats
(Elsevier B. V., 2014) Omobowale, T. O.; Oyagbemi, A. A.; Akinrinde, A. S.; Saba, A. B.; Daramola, O. T.; Ogunpolu, B. S.; Olopade, J. O.
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 H2O2 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.
Failure of recovery from lead induced hepatoxicity and disruption of erythrocyte antioxidant defence system in Wistar ratsTemidayo
(Elsevier B.V., 2014) Omobowale, T. O.; Oyagbemi, A. A.; Akinrinde, A. S.; Saba, A. B.; Daramola, O. T.; Ogunpolu, B. S.; Olopade, J. O.
Lead acetate (PbA) is one of the major environmental contaminants with grave toxicologicalconsequences both in the developing and developed countries. The liver and erythrocyteantioxidant status and markers of oxidative were assessed. Exposure of rats to PbA ledto significant decline (p < 0.05) in hepatic and erythrocyte glutathione peroxidase (GPx),glutathione S-transferase (GST), catalase (CAT), superoxide dismutase (SOD), and reducedglutathione (GSH) content. Similarly, malondialdehyde (MDA) and H2O2concentrations weresignificantly (p < 0.05) elevated. Histopathology and immunohistology of liver of rats exposedto 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 afterwithdrawal of the exposed PbA for the period of the study. In conclusion, experimentalanimals exposed to PbA did not recover from hepatotoxicity and disruption of erythrocyteantioxidant defence system via free radical generation and oxidative stress.
In vitro cytotoxicity activity of the methanol leaf extract of Picralima nitida on human colorectal adenocarcinoma cell lines (HT-29)
(AkiNik Publications, 2021) Adedapo, A. A.; Yusuff, A. A.; Falayi, O. O.; Ogunmiluyi, I. O.; Ogunpolu, B. S.; Omobowale, T. O.; Oyagbemi, A. A.; Adejumobi, O. A.; Oguntibeju, O. O.; Yakubu, M. A.; Yakubu, F. B.
The anti-proliferative effect of the methanol leaf extract of Picralima nitida on Human Colorectal Adenocarcinoma Cell lines (HT-29) was investigated using the Cell Titer 96 MTT assay because Picralima nitida is a therapeutic herb used in ethnomedicine for the management of several disease conditions. Cells were cultured to confluence, trypsinized, and plated in 96-well plates for cell proliferation assay. Twenty four hours after plating, cells were treated with various concentrations (62.5, 125, 250 μm) of the extract along with the control in the presence or absence of Calphostin C (10 μm) or Tyrphostin (10 μm) and cultured for 24–72 h to determine effects of treatment on cell growth. MTT assay was performed at 24, 48 and 72. MTT assay was performed over 3 days. In vitro antiproliferative study showed that the extract at all concentrations caused cytotoxicity of the HT29 cells. The extract in the absence of the enzyme inhibitors caused a higher cell inhibition than in their presence with the 62.5 μm/ml causing a higher inhibitory effect on the cells. The ability of the methanol leaf extract of Picralima nitida with a higher antiproliferative property in the absence of the enzyme inhibitors is a pointer to its cytotoxic efficacy. It was thus concluded from this study that the plant extract from Picralima nitida has anti-proliferative/cytotoxic effect hence further evaluation on the constituents responsible for this effect may be explored.
Lack of reversal of oxidative damage in renal tissues of lead Acetate-treated rats
(Wiley, 2014) Oyagbemi, A. A.; Omobowale, T. O.; Akinrinde, A. S.; Saba, A. B.; Ogunpolu, B. S.; Daramola, O.
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<0.05) in a dosedependent manner, whereas reduced glutathione (GSH) level and glutathione peroxidase activity were significantly reduced. The pattern of alterations in most of the oxidative stress and antioxidant parameters remained similar in rats from the withdrawal period, although CAT and SOD activities reduced, in contrast to their elevation during the exposure period. Serum creatinine levels were significantly elevated in both exposure and withdrawal experiments whereas serum blood urea nitrogen levels were not significantly different from the control in both exposure and withdrawal periods. The histological damage observed include multifocal areas of inflammation, disseminated tubular necrosis, and fatty infiltration of the kidney tubules both at exposure and withdrawal periods. The results suggest that lead acetate-induced nephrotoxicity by induction of oxidative stress and disruption of antioxidant. The aforementioned alterations were not reversed in the rats left to recover within the time course of study.
Lack of reversal of oxidative damage in renal tissues of Lead Acetate-Treated rats
(Wiley Periodicals, Inc., 2014) Oyagbemi, A. A.; Omobowale, T. O.; Akinrinde, A. S.; Saba, A. B.; Ogunpolu, B. S.; Daramola, O.
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 < 0.05) in a dose dependent manner, whereas reduced glutathione (GSH) level and glutathione peroxidase activity were significantly reduced. The pattern of alterations in most of the oxidative stress and antioxidant parameters remained similar in rats from the withdrawal period, although CAT and SOD activities reduced, in contrast to their elevation during the exposure period. Serum creatinine levels were significantly elevated in both exposure and withdrawal experiments whereas serum blood urea nitrogen levels were not significantly different from the control in both exposure and withdrawal periods. The histological damage observed include multifocal areas of inflammation, disseminated tubular necrosis, and fatty infiltration of the kidney tubules both at exposure and withdrawal periods. The results suggest that lead acetate-induced nephrotoxicity by induction of oxidative stress and disruption of anti-oxidant. The aforementioned alterations were not reversed in the rats left to recover within the time course of study.
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.
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.
Persea americana bark extract modulates Nω-nitro-L-arginine methyl ester (L-NAME)-induced hypertension through NF-κB/Nrf2/KIM-1/cTnI signaling pathways in Wistar rats.
(Physiological Society of Nigeria, 2025) Adejumobi, O. A.; Oriaku, V.; Gbadegoye, J. O.; Afolabi, J. M.; Ogunpolu, B. S.; Ajani, T. F.; Omotosho, O. O.; Ohore, O. G.; Oyagbemi, A. A.; Adedapo, A. A.; Yakubu, M. A.; Ashafa, A. O. T.; Nottidge, H. O.; Omobowale, T. O.
Hypertension is one of the major risk factors for cardiovascular diseases. It has become a significant public health concern in both developed and developing countries. In this study we evaluated the ameliorative effect of methanol bark extract of Persea americana (PA) on L-NAME-induced hypertension and its attendant cardiac and renal complications. Sixty rats were divided into six groups. Group A was the negative control and received distilled water throughout the sturdy. Group B received a daily repetitive dose of L-NAME alone at 40 mg/kg for 21 days. Groups C, D, and E received a daily repetitive dose of L-NAME at 40 mg/kg and extract at 100 mg/kg. 200 mg/kg and 400 mg/kg, respectively, for 21 days. Group F received a daily repetitive dose of L-NAME at 40 mg/kg and lisinopril at 10 mg/kg for 21 days. The results showed that L-NAME significantly elevated blood pressure, markers of renal damage, oxidative stress, and expression of KIM-1, NRF2, NF-KB and CTnl, while it decreased both enzymatic and non-enzymatic antioxidant parameters. The extract and lisinopril, however, ameliorated these effects in the rat model. These findings showed that the bark extract of PA may play a role in reducing oxidative stress, inflammation, cardio-renal organ damage and blood pressure levels in hypertension, possibly through free radical scavenging, antioxidant system potentiation, NF-kB/NRF2/KIM-1/CTnI signaling pathways.
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.
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
The methanol leaf extract of Picralima nitida mitigates cisplatin-induced toxicities in rats through nuclear factor kappa B, cardiac troponin, mineralocorticoid receptor, and Nrf2 signaling pathways.
(Shahrekord University of Medical Sciences, 2022) Adedapo, A. A.; Yosuf, A. A.; Falayi, O. O.; Ogunmiluyi, I. O.; Ogunpolu, B. S.; Omobowale, T. O.; Oyagbemi, A. A.; Adejumobi, O. A.; Oguntibeju, O. O.; Yakubu, M. A.; Yakubu, F. B.
Introduction: Cisplatin (CP)-induced toxicity involves oxidative stress and Picralima nitida is rich in natural antioxidants hence its methanol leaf extract was used to mitigate the toxic effect of CP. Methods: Forty rats divided into four groups of 10 rats per group were used as follows: group A (normal saline), group B (CP 10 mg/kg), group C [Methanol Leaf Extract of Picralima nitida (MLEPN), 100 mg/kg and CP 10 mg/kg], and group D (MLEPN 200 mg/kg and CP 10 mg/kg). All administrations were done by oral gavage with the volumes of the treatments administered determined by the average weight of the rats in each group except CP, which was given intraperitoneally. Administration of normal saline and MLEPN lasted for seven consecutive days after which a single dose of CP was given on day 8. All animals were sacrificed 72 hours after CP administration. On day 9, blood pressure measurement was taken, and changes in body weight were determined. On day 10, blood samples were taken for serum chemistry, and kidneys, liver, and heart were harvested from the animals for serum assay, histopathology, and immunohistochemistry, respectively. Results: The extract improved weight changes caused by CP and reversed the toxic changes produced by CP on serum chemistry, oxidative stress, and histopathology. The extract caused a significant decrease in the levels of nuclear factor kappa beta, cardiac troponin, and mineralocorticoid receptors (MCRs). However, it increased the protein expression of Nrf2 compared to the toxicant group. Conclusion: The extract exhibited anti-inflammatory, antioxidant, and anti-renin properties.