Browsing by Author "Omobowale, T. O."

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A Case of Craniothoracopagus (Monocephalus Thoracopagus Tetrabrachius) in a Dog
(Blackwell Verlag, 2007) Nottidge, H. O.; Omobowale, T. O.; Olopade, J. O.; Oladiran, O. O.; Ajala, O. O.
This report describes a case of craniothoracopagus (mon cephalus thoracopagus tetrabrachius) twin puppies in Ibadan, Nigeria. The conjoined twins were given birth to by a 7-year old bitch that was usually allowed to stray away from home in search of food. Deformities of the cardiovascular, digestive musculoskeletal, respiratory and urinary systems are reported. This is probably the first report of craniothoracopagus twinning in a dog.
Alchornea laxiflora (Benth.) Pax & K. Hoffman extract protects against lead-induced neurodegeneration in cockerel chickens.
(Elsevier Inc. on behalf of International Brain Research Organization, 2024) Esan, O. O.; Igado, O. O.; Femi-Akinlosotu, O. M.; Oyagbemi, A. A.; Omobowale, T. O.; Oladele, O. A.; Nwulia, E.
Lead (Pb) is a ubiquitous, non-biodegradable heavy metal contaminant with a significant impact on both human and animal health. The adverse effect of lead on health and productivity of avian species has received little attention. Alchornea laxiflora (Benth) belongs to Euphorbiaceae family and grows naturally in the Nigerian rain forest. Decoction of the leaves is usually administered traditionally to treat inflammatory and infectious diseases. The ethanol extract of Alchornea laxiflora (EaAL) leaves was used in this study to ameliorate lead-induced neurodegeneration. Seven groups of 5-week-old cockerels (n=5) were treated for 6 weeks thus: Group A - Control (water only), Group B - (100 mg/kg of EaAL daily), Group C - (200 mg/kg of EaAL daily, p.o.), Group D - (1 % lead acetate in drinking water), Group E - (1 % lead acetate in drinking water and 100 mg/kg of EaAL daily), Group F - (1 % lead acetate and 200 mg/kg of EaAL daily), Group G - (1 % lead acetate and 100 mg/kg of Vitamin C). All administrations were per os birds were euthanized on day 43 by quick cervical dislocation. Histological stains (H&E and Nissl) and Black Gold II (BGII) histochemistry were used to assess alterations in the cerebrum and cerebellum. Administration of EaAL at the two concentrations resulted in a drastic reduction in the incidence of neuro pathologies observed (e.g. pyknosis and multilayering of Purkinje cells, neuronal degeneration in hippocampus cerebrum and ependymal cells, distortion of meningeal epithelial cells, etc). BGII histochemistry revealed severe demyelination caused by the administration of lead acetate, while the two doses of EaAL showed significant restoration of myelin in the cerebellum. The amelioration of demyelination observed with the use of vitamin C was considerably lower than that recorded with the use of EaAL. The use of EaAL significantly ameliorated morphological alterations and demyelination caused by the administration of lead acetate, however, caution should be exercised in the administration, as individual species idiosyncrasies may arise and the tendency to pro-oxidation at 200 mg/kg when administered alone was observed in one subject.
Alleviation of oxidized lipid-induced oxidative stress and hypertension by estrogen and selected antihyperlipidemic drugs in postmenopausal Wistar rats
(INNOSC (Innovative Space of Scientific Research), 2024) Folahan, J. T.; Oyewopo, A. O.; Adejumobi, O. A.; Ajayi, A. M.; Afolabi, S. O.; Atolani, O. O.; Ologe, M. O.; Omobowale, T. O.; Olorundare, O. E.
Lipid peroxidation is implicated in the development of hypertension and coronary artery disease, and its deleterious impact is exacerbated by estrogen (ETD) depletion in post-menopausal women. We hypothesize that treatment with ETD and antihyperlipidemic drugs, either alone or in combination, can alleviate the development of cardiovascular disease. In this study, female Wistar rats were divided into 10 groups (n = 6): Group 1 (control) underwent a Sham operation and was fed standard rat chow, whereas the other nine groups were ovariectomized (OVX) and received a diet containing either thermoxidized palm oil (TPO) or thermoxidized soya oil (TSO) for 12 weeks. ETD at 0.2 mg/kg/day, atorvastatin (ATV) at 10 mg/kg/day, and a combination of ezetimibe (EZE) and ATV (EZE at 3 mg/kg/day + ATV at 10 mg/kg/day) were administered for 12 weeks in both TSO and TPO diet groups. Blood pressure and electrocardiogram (ECG) parameters were assessed, along with serum lipid profile, atherogenic indices, and markers of oxidative stress. Both TPO and TSO diets significantly altered blood pressure and ECG parameters in OVX rats. Treatment with ATV, EZE+ATV, and ETD significantly reduced blood pressure parameters compared to the OVX+TPO group. Antihyperlipidemic drugs significantly decreased heart rate, QT interval, QRS duration, and QT corrected (QTc), whereas ETD similarly shortened the QRS and QTc duration. ATV and ETD also reduced total cholesterol, triglycerides, and very low-density lipoprotein levels, while boosting high-density lipoprotein concentrations compared to untreated OVX+TSO rats. This study demonstrates that thermoxidized oil has a deleterious effect on OVX rats by altering blood pressure, ECG parameters, and atherogenic indices. Treatment with antihyperlipidemic drugs and ETD normalized blood pressure and ECG parameters, reversed hyperlipidemia, and restored antioxidant system balance.
Alterations in blood pressure, antioxidant status and caspase 8 expression in cobalt chloride-induced cardio-renal dysfunction are reversed by Ocimum gratissimum and gallic acid in Wistar rats
(Elsevier GmbH, 2016) Akinrinde, A. S.; Oyagbemi, A. A.; Omobowale, T. O.; Asenuga, E. R.; Ajibade, T. O.
The protective abilities of the chloroform extract of Ocimum gratissimum (COG) and gallic acid against cobalt chloride (CoCl2) − induced cardiac and renal toxicity were evaluated. Rats were exposed to CoCl2 (350 ppm) for 7 days, either alone, or in combination with COG (100 and 200 mg/kg) or gallic acid (120 mg/kg). CoCl2 given alone, caused significant increases (p < 0.05) in oxidative stress parameters (hydrogen peroxide, H2O2 and malondialdehyde, MDA) and increased expression of the apoptotic initiator caspase 8 in the heart and kidneys. There was significant reduction (p < 0.05) in reduced glutathione (GSH) in cardiac and renal tissues; reduction in superoxide dismutase (SOD) activity in the kidneys and adaptive increases in Glutathione S-transferase (GST) and catalase (CAT). CoCl2 also produced significant reduction (p < 0.05) in systolic (SBP), diastolic (DBP) and mean arterial (MAP) blood pressures. Oral COG and gallic acid treatment significantly reduced (p < 0.05) the levels of H2O2 and MDA; with reduced expression of caspase 8 and restoration of GSH levels, GPx, SOD and CAT activities, howbeit, to varying degrees in the heart and kidneys. COG (200 mg/kg) was most effective in restoring the blood pressures in the rats to near control levels. CoCl2-induced histopathological lesions including myocardial infarction and inflammation and renaltubular necrosis and inflammation were effectively ameliorated by the treatments administered. This study provides evidence for the protective roles of O. gratissimum and gallic acid by modulation of CoCl2-induced alterations in blood pressure, antioxidant status and pro-apoptotic caspase 8 in Wistar rats.
Alterations in blood pressure, antioxidant status and caspase 8expression in cobalt chloride-induced cardio-renal dysfunction arereversed by Ocimum gratissimum and gallic acid in Wistar rats
(Elsevier B.V., 2016) Akinrinde, A. S.; Oyagbemi, A. A.; Omobowale, T. O.; Asenuga, E. R.; Ajibade, T. O.
The protective abilities of the chloroform extract of Ocimum gratissimum (COG) and gallic acid againstcobalt chloride (CoCl2) − induced cardiac and renal toxicity were evaluated. Rats were exposed to CoCl2(350 ppm) for 7 days, either alone, or in combination with COG (100 and 200 mg/kg) or gallic acid(120 mg/kg). CoCl2given alone, caused significant increases (p < 0.05) in oxidative stress parameters(hydrogen peroxide, H2O2and malondialdehyde, MDA) and increased expression of the apoptotic initia-tor caspase 8 in the heart and kidneys. There was significant reduction (p < 0.05) in reduced glutathione(GSH) in cardiac and renal tissues; reduction in superoxide dismutase (SOD) activity in the kidneys andadaptive increases in Glutathione S-transferase (GST) and catalase (CAT). CoCl2also produced signifi-cant reduction (p < 0.05) in systolic (SBP), diastolic (DBP) and mean arterial (MAP) blood pressures. OralCOG and gallic acid treatment significantly reduced (p < 0.05) the levels of H2O2and MDA; with reducedexpression of caspase 8 and restoration of GSH levels, GPx, SOD and CAT activities, howbeit, to varyingdegrees in the heart and kidneys. COG (200 mg/kg) was most effective in restoring the blood pressures inthe rats to near control levels. CoCl2-induced histopathological lesions including myocardial infarctionand inflammation and renal tubular necrosis and inflammation were effectively ameliorated by the treat-ments administered. This study provides evidence for the protective roles of O. gratissimum and gallicacid by modulation of CoCl2-induced alterations in blood pressure, antioxidant status and pro-apoptoticcaspase 8 in Wistar rats.
Ameliorative effect of gallic acid in doxorubicin-induced hepatotoxicity in wistar rats through antioxidant defense system
(Taylor & Francis, 2017-07) Omobowale, T. O.; Oyagbemi, A. A.; Ajufo, U. E.; Adejumobi, A. O.; Ola-Davies, O. E.; Adedapo, A. A.; Yakubu, M. A.
Hepatotoxicity has been found to be one of the main side effects associated with doxorubicin (Dox) administration in cancer therapy. The aim of the present study was to examine the ameliorative effect of gallic acid (GA) in Dox-induced hepatotoxicity. Sixty male Wistar rats of 10 rats per group were used in this study and were randomly divided into 6 experimental groups (A–F). Rats in Group A served as the control group and received distilled water orally for 7 days; Group B was given Dox at 15 mg/kg bodyweight intraperitoneally (IP) on Day 8. Group Cwas given GA at 60 mg/kg body weight orally for 7 days + Dox at 15 mg/kg IP on Day 8. Group D was given GA at 120 mg/kg body weight orally for 7 days +Dox at 15 mg/kg IP on day 8. Rats in Groups E and F were administered GA alone at 60 and 120 mg/kg bodyweight orally for 7 days, respectively. Dox administration led to a significant reduction in hepatic reduced glutathione and nonprotein thiol (NPT) together with significant increase in hepatic malondialdehyde, hydrogen peroxide generation, superoxide dismutase, and catalase activity; hepatic glutathione peroxidase and glutathione-S-transferase activity were significantly inhibited in Dox-treated rats. The serum alanine aminotransferase (ALT), alkaline phosphatase, and total bilirubin concentrations were significantly elevated following Dox administration. Pretreatment with GA ameliorated Dox-induced hepatotoxicity and oxidative stress. The results suggest that GA may offer protection against hepatic damage in Dox cancer chemotherapy.
Ameliorative Effect of Gallic Acid on Doxorubicin- Induced Hepatotoxicity in Wistar Rats Through Antioxidant Defence System
(Taylor & Francis, 2018) Omobowale, T. O.; Oyagbemi, A. A.; Ajufo, U. E.; Adejumobi, O. A.; Ola-Davies, O. E.; Adedapo, A. A.; Yakubu, M. A.
Hepatotoxicity has been found to be one of the main side effects asso- ciated with doxorubicin (Dox) administration in cancer therapy. The aim of the present study was to examine the ameliorative effect of gallic acid (GA) in Dox-induced hepatotoxicity. Sixty male Wistar rats of 10 rats per group were used in this study and were randomly divided into 6 experimental groups (A-F). Rats in Group A served as the control group and received distilled water orally for 7 days: Group B was given Dox at 15 mg/kg body weight intraperitoneally (IP) on Day 8. Group C was given GA at 60 mg/kg body weight orally for 7 days + Dox at 15 mg/kg IP on Day 8. Group D was given GA at 120 mg/kg body weight orally for 7 days +Dox at 15 mg/kg IP on day 8. Rats in Groups E and F were administered GA alone at 60 and 120 mg/kg body weight orally for 7 days, respectively. Dox administration led to a significant reduction in hepatic reduced glu- tathione and nonprotein thiol (NPT) together with significant increase in hepatic malondialdehyde, hydrogen peroxide generation, superax- ide dismutase, and catalase activity; hepatic glutathione peroxidase and glutathione-S-transferase activity were significantly inhibited in Dox-treated rats, The serum alanine aminotransferase (ALT), alkaline phosphatase, and total bilirubin concentrations were significantly ele- vated following Dox administration. Pretreatment with GA ameliorated Dox-induced hepatotoxicity and oxidative stress. The results suggest that GA may offer protection against hepatic damage in Dox cancer chemotherapy.
Ameliorative effect of gallic acid on doxorubicin-induced cardiac dysfunction in rats
(De Gruyter, 2017) Omobowale, T. O.; Oyagbemi, A. A.; Folasire, A. F.; Ajibade, T. O.; Asentiga, E. R.; Adejumobi, O. A.; Ola-Davies, O. E.; Oyetola, O.; James, G.; Adedapo, A. A.; Yakubu, M. A.
Background: The use of doxorubicin (DOX) as an antineoplastic agent has been greatly limited because of the myriad of toxic sequelae associated with it. The aim of this study was to assess the protective effects of gallic acid (GA) on DOX-induced cardiac toxicity in rats. Methods: Sixty male rats (Wistar strain) were used in this study. They were divided into six groups (A–F) each containing 10 animals. Group A was the control. Rats in Groups B, C, and D were treated with DOX at the dosage of 15 mg/kg body weight i.p. Prior to this treatment, rats in Groups C and D had been treated orally with GA for 7 days at the dosage of 60 and 120 mg/kg, respectively. Animals from Groups E and F received only 60 and 120 mg/kg GA, respectively, which were administered orally for 7 days. Results: The exposure of rats to DOX led to a significant (p 0.05) decrease in the cardiac antioxidant defence system and elevation of creatine kinase myocardial band and lactate dehydrogenase. The electrocardiography results showed a significant decrease in heart rate, QRS, and QT-segment prolongation. GA alone improved the antioxidant defence system. Conclusions: The GA pretreatment significantly alleviated GA-associated ECG abnormalities, restored the antioxidant status and prevented cardiac damage.
Ameliorative Effect of Garlic Acid on Doxorubicin-Induced Cardiac Dysfunction in Rats
(Walter de Gruyter GmbH, 2018) Omobowale, T. O.; Oyagbemi, A. A.; Folasire, A. M.; Ajibade, T. O.; Asenuga, E. R.; Adejumobi, O. A.; Ola-Davies, O. E.; Oyetola, O.; James, G.; Adedapo, A. A.; Yakubu, M. A.
Background: The use of doxorubicin (DOX) as an anti- neoplastic agent has been greatly limited because of the myriad of toxic sequelae associated with it. The aim of this study was to assess the protective effects of gallic acid (GA) on DOX-induced cardiac toxicity in rats. Methods: Sixty male rats (Wistar strain) were used in this study. They were divided into six groups (A-F) each containing 10 animals. Group A was the control. Rats in Groups B, C, and D were treated with DOX at the dosage of 15 mg/kg body weight i.p. Prior to this treatment, rats in Groups C and D had been treated orally with GA for 7 days at the dosage of 60 and 120 mg/kg, respectively. Animals from Groups E and F received only 60 and 120 mg/kg GA, respectively, which were administered orally for 7 days Results: The exposure of rats to DOX led to a significant Received December 27, 2016; accepted July 23, 2017; previously (p<0.05) decrease in the cardiac antioxidant defence published online October 9, 2017 Abstract Background: The use of doxorubicin (DOX) as an anti- neoplastic agent has been greatly limited because of the myriad of toxic sequelae associated with it. The aim of this study was to assess the protective effects of gallic acid (GA) on DOX-induced cardiac toxicity in rats. Conclusions: The GA pretreatment significantly alleviated GA-associated ECG abnormalities, restored the antioxi dant status and prevented cardiac damage.
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.
Antioxidant and antihypertensive effects of methanol leaf extract of Ficus exasperata on Nω-nitro-L-arginine methyl ester (L-NAME)-induced hypertension and oxidative stress in rats
(International Organization of Scientific Research, 2024) Adejumobi, O. A.; Akinbobe, E. S.; Omotosho, O. O.; Olakojo, T. A.; Ajani, T. F.; Oyagbemi, A. A.; Adedapo, A. A.; Yakubu, M.; Ashafa, A. O. T.; Nottidge, H. O.; Omobowale, T. O.
Chemopreventive effect of ethanolic extract of azadiractha indica on experimental trypanosoma brucei induced oxidative stress in dogs
(Phcog.Net, 2015) Omobowale, T. O.; Oyagbemi, A. A.; Oyewunmi, O. A.; Adejumobi, O. A.
The medicinal properties of Azadirachta indica have boen harnessed for many years in the treatment of many diseases in both humans and animals. Materials and Methods: Twenty-five apparently healthy dogs weighing between 3 and 8 kg were randomly divided into five groups with five dogs in each group. Ameliorative effect of A. indica on erythrocyte anpioxidant status and markers of oxidative stress were assessed. Liver artd kidney function tests were also performed. Results: Pre-treatment with methanolic extract af Azadirachta indica IMEA at different doses did not significantly alter the values of alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase activity in Trypanosoma brucel infection. Although, serum creatinine significantly (P < 0.05) decreased with pre-treatment with 50 mg/kg A. indice, after 2 weeks of 7. brucelintection. However, the reduced glutathione (GSH) content of the erythrocyte increased significantly in animals pre-treated with 50 mg/kg and 200 mg/kg of A. indica respectively. Markers of oxidative stress such as malond aldehyde and hydrogen peroxide generated were higher in animals infected with 7. brucel with no significant (P>0.051 difference compared to the values obtained in pre-treated animals. Pre treatment with 100 mg/kg and 200 mg/kg of A. indica significantly (P < 0.05) decreased serum myeloperoxidase activity at 2 weeks post-infection with 7. brucel. Conclusion: From this study. MEAI showed significant ability to attenuate oxidative stress and inflammation during experimental T. brucei infection.
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.
Cobalt chloride-induced hepatic and intestinal damage in rats: protection by ethyl acetate and chloroform fractions of Ocimum gratissimum
(Informatics Publishing Limited, 2016) Akinrinde, A. S.; Oyagbemi, A. A.; Omobowale, T. O.; Nwozuzu, V. C.
Cobalt chloride is known to produce symptoms of diarrhea, vomiting and other gastrointestinal disturbances. We investigated the potential roles of the ethyl acetate and chloroform fractions of Ocimum gratissimum (OG), traditionally used to treat diarrhea and other gastrointestinal disorders in protection against cobalt chloride (CoCl2)-induced liver and intestinal damage. Wistar albino rats were given CoCl2 (350 ppm) in drinking water for 7 days, alone or concurrently with either fractions of OG at 100 and 200mg/kg each. Gallic acid (120 mg/kg) was administered to a group of rats as a standard flavonoid. Biochemical indices of oxidative stress, antioxidant enzyme activities, the levels of pro-inflammatory cytokines (Interleukin 1β; IL-1β and Tumor necrosis factor, TNF-α) were evaluated and the histological appearance of the liver and intestinal mucosa was investigated. CoCl2 produced significant elevations (p<0.05) in hydrogen peroxide (H2O2), malondialdehyde (MDA), IL-1β, alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase (ALP). This was accompanied with significant reductions (p<0.05) in reduced glutathione (GSH), glutathione peroxidase (GPX) and glutathione S-transferase (GST) activities. Liver sections of rats exposed to CoCl2 had poor architecture and areas of necrosis with several dead hepatocytes, while some appeared with hyperchromic nuclei. Intestinal mucosa showed significant loss of absorptive epithelial cells with CoCl2 exposure. Treatment with the fractions from OG produced reduction in H2O2, MDA and IL-1β levels; reduced serum activities of ALT, AST and ALP; restoration of GSH levels and improved activities of GPX and GST. The fractions significantly preserved the hepatic and intestinal architecture.Our results indicate that the fractions of OG exhibited considerable hepatic and intestinal protection by reduction in levels of oxidants and pro-inflammatory cytokines, enhancement of antioxidant enzyme activities and preservation of tissue integrity and might thus be very useful agents in protecting the liver and intestines during concurrent exposure to Cobalt chloride.