FACULTY OF VETERINARY MEDICINE
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Item 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 bioavailabilityItem 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.Item Enalapril confers protective effect on isoproterenol-induced myocardial infarction in rats through down regulation of cardiac troponin, c-reactive protein, upregulation of il-10β as well as anti-oxidant and anti-inflammatory activities.(Sciencedomain International, 2018) Adeoye, B.; Ajibade, T. O.; Asenuga, E.; Adejumobi, O. A.; Oyagbemi, A. A.; Omobowale, T. O.; Adedapo, A.Myocardial infarction is an irreversible death of heart muscle secondary due to prolonged lack of oxygen supply. The present study was designed to evaluate the protective effect of enalapril in isoproterenol-induced myocardial infarction in rats using changes in haemodynamic, biochemical, histopathological and immunohistochemistry parameters. Twenty-one male Wistar rats divided into three groups were used where the control (group A) was administered for normal saline which continued for 7 days, group B animals received normal saline for 7 days and thereafter isoproterenol (ISO) at 85 mg/kg on day 8 and 9. Group C animals were pretreated with enalapril (10 mg/kg) for 7 days and thereafter received ISO on day 8 and 9. On day 10, the blood pressure change in the animals were measured and thereafter sacrificed by cervical dislocation. The heart of each rat was removed, homogenized and used to assay for some oxidative stress markers and some antioxidant parameters. In this study, ISO caused myocardial infarction as seen by significant decrease in systolic, diastolic and mean arterial pressure but was corrected by enalapril, Enalapril caused significant increase in the levels of SOD, GPX, GST and GSH but significant decrease in MDA content and HO2 generation. But reverse was the case for group B animals. Immunohistochemistry showed that ISO caused higher expressions of cardiac C-reactive protein (CRP) and cardiac troponins 1 (CTn1) and decrease in IL-10ẞ but vice-versa for enalapril. No histopathological changes were recorded for enalapril. The study thus showed that enalapril significantly exhibits cardioprotective effects.Item 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.Item Cyclophosphamide‑induced hepatotoxicity in Wistar rats: The modulatory role of Gallic Acid as a hepatoprotective and chemopreventive phytochemical(Wolters Kluwer - Medknow, 2016) Oyagbemi, A. A.; Omobowale, O. T.; Asenuga, E. R.; Akinleye, A. S.; Ogunsanwo, R. O.; Saba, A. B.Background: Gallic acid (GA) is an endogenous plant phenol known to have antioxidant, free radical scavenging ability, anti inflammatory, anti cancer, and anti fungal properties. The aim of this study was to assess the protective effect of GA on cyclophosphamide (CPA) induced hepatotoxicity in male Wistar rats. Methods: Sixty rats were grouped into six groups of 10 rats per group. Group 1 received distilled water. Group 2 received CPA at 200 mg/kg single dose intraperitoneally on day 1. Groups 3 and 4 received a single dose of CPA (200 mg/kg) intraperitoneally on day 1 and then were treated with GA at 60 and 120 mg/kg body weight for 14 days, respectively. Rats in Groups 5 and 6 only received GA at 60 and 120 mg/kg body weight for 14 days, respectively. GA was administered orally. Results: CPA induced hepatic damage as indicated by significant elevation (P < 0.05) in aspartate aminotransferase, organ weight, and evidence by the histological study. CPA also induced hepatic oxidative stress as indicated by significant elevation (P < 0.05) in malondialdehyde content, hydrogen peroxide (H2 O2 ) generation, nitrite level, and the level of glutathione (GSH) peroxidase crashed in the CPA treated group. GA enhanced the antioxidant defense system as indicated by significant elevation (P < 0.05) in GSH level, catalase activity, and GSH S transferase activity. Conclusions: Taken together, the result of this present study shows that GA has a protective effect on CPA induced hepatotoxicity.Item Gallic acid protects against cyclophosphamide-induced toxicity in testis and epididymis of rats(Blackwell Verlag GmbH, 2015) Oyagbemi, A. A.; Omobowale, T. O.; Saba, A. B.; Adedara, I. A.; Olowu, E. R.; Akinrinde, A. S.; Dada, R. O.The protective role of gallic acid (GA) on reproductive toxicity induced by cyclophosphamide (CPA), an antineoplastic drug, was investigated in male Wistar rats. Sixty rats were grouped into 10 rats per group. Group 1 (control) received distilled water. Rats in groups 2 and 3 received GA alone at 60 and 120 mg kg 1 for 14 consecutive days, respectively. Group 4 received a single intraperitoneal dose of CPA at 200 mg kg 1 on day 1. Groups 5 and 6 received a single dose of CPA (200 mg kg 1 ) intraperitoneally on day 1 followed by treatment with GA at 60 and 120 mg kg 1 for 14 consecutive days, respectively. In testes and epididymis of the treated rats, CPA administration resulted in significant elevation (P < 0.05) in malondialdehyde (MDA), nitrite and hydrogen peroxide levels. There was a significant decrease in the activities of superoxide dismutase and glutathione-S-transferase. Furthermore, there were significant reductions in plasma luteinising hormone (LH), follicle stimulation hormone (FSH) and testosterone levels, which were accompanied by significant decrease in sperm motility and viability in CPA-treated rats. Histological examination revealed marked testicular and epididymal atrophy in CPA alone trea ted rats and these aberrations were reversed by GA. In conclusion, GA has capacity to protect against reproductive toxicity induced by cyclophosphamide.Item Cyclophosphamide‑induced hepatotoxicity in Wistar Rats: the modulatory role of Gallic Acid as a hepatoprotective and Chemopreventive phytochemical(Medknow Publications, 2016) Oyagbemi, A. A.; Omobowale, O. T.; Asenuga, E. R.; Akinrinde, S. A.; Ogunsanwo, R. O.; Saba, A. B.Background: Gallic acid (GA) is an endogenous plant phenol known to have antioxidant, free radical scavenging ability, anti‑inflammatory, anti‑cancer, and anti‑fungal properties. The aim of this study was to assess the protective effect of GA on cyclophosphamide (CPA)‑induced hepatotoxicity in male Wistar rats. Methods: Sixty rats were grouped into six groups of 10 rats per group. Group 1 received distilled water. Group 2 received CPA at 200 mg/kg single dose intraperitoneally on day 1. Groups 3 and 4 received a single dose of CPA (200 mg/kg) intraperitoneally on day 1 and then were treated with GA at 60 and 120 mg/kg body weight for 14 days, respectively. Rats in Groups 5 and 6 only received GA at 60 and 120 mg/kg body weight for 14 days, respectively. GA was administered orally. Results: CPA induced hepatic damage as indicated by significant elevation (P < 0.05) in aspartate aminotransferase, organ weight, and evidence by the histological study. CPA also induced hepatic oxidative stress as indicated by significant elevation (P < 0.05) in malondialdehyde content, hydrogen peroxide (H2O2) generation, nitrite level, and the level of glutathione (GSH) peroxidase crashed in the CPA‑treated group. GA enhanced the antioxidant defense system as indicated by significant elevation (P < 0.05) in GSH level, catalase activity, and GSH‑S‑transferase activity. Conclusions: Taken together, the result of this present study shows that GA has a protective effect on CPA‑induced hepatotoxicity.Item Gallic acid protects against cyclophosphamide-induced toxicity in testis and epididymis of rats(Blackwell Verlag GmbH, 2015) Oyagbemi, A. A.; Omobowale, T. O.; Saba, A. B.; Adedara, I. A.; Olowu, E. R.; Akinrinde, A. S.; Dada, R. O.The protective role of gallic acid (GA) on reproductive toxicity induced by cyclophosphamide (CPA), an antineoplastic drug, was investigated in male Wistar rats. Sixty rats were grouped into 10 rats per group. Group 1 (control) received distilled water. Rats in groups 2 and 3 received GA alone at 60 and 120 mg kg _1 for 14 consecutive days, respectively. Group 4 received a single intraperitoneal dose of CPA at 200 mg kg _1 on day 1. Groups 5 and 6 received a single dose of CPA (200 mg kg _1) intraperitoneally on day 1 followed by treatment with GA at 60 and 120 mg kg _1 for 14 consecutive days, respectively. In testes and epididymis of the treated rats, CPA administration resulted in significant elevation (P < 0.05) in malondialdehyde (MDA), nitrite and hydrogen peroxide levels. There was a significant decrease in the activities of superoxide dismutase and glutathione-S-transferase. Furthermore, there were significant reductions in plasma luteinising hormone (LH), follicle stimulation hormone (FSH) and testosterone levels, which were accompanied by significant decrease in sperm motility and viability in CPA-treated rats. Histological examination revealed marked testicular and epididymal atrophy in CPA alone treated rats and these aberrations were reversed by GA. In conclusion, GA has capacity to protect against reproductive toxicity induced by cyclophosphamide.Item 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.Item 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.