Veterinary Medicine
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Item Ethanol extract of Ficus exasperata leaf and gallic acid ameliorate cisplatin-induced toxicity in Wistar rats(Science Publishing Group, 2025) Adejumobi, O. A.; Oloko, M. D.; Omotosho, O. A.; Abiola, J. O.; Banwo, O. G.; Akinniyi, O. O.; Ajani, T. F.; Oyagbemi, A. A.; Adedapo, A. A.; Yakubu, M. A.; Omóbòwálé, T. O.Cisplatin (CP), a widely used platinum-based chemotherapeutic, is effective in cancer treatment but it is associated with significant multiple organ toxicity, particularly the liver, kidneys, gastrointestinal tract, and cardiovascular system. Oxidative stress is a major contributor to this toxicity. This study aimed to investigate the protective effects of Ficus exasperata (FE) extract and gallic acid (GA), both known for their antioxidant properties, against cisplatin-induced toxicity, oxidative stress, and organ damage in Wistar rats. Fifty male Wistar rats (162–266 g) were randomly assigned to five groups (A–E; n=10). Group A received distilled water only (control). Group B was administered cisplatin (10 mg/kg, intraperitoneally) on day 8. Groups C and D received 100 mg/kg and 200 mg/kg of Ficus exasperata extract orally for 8 days, respectively, followed by cisplatin administration on day 8. Group E received gallic acid (100 mg/kg orally) for 8 days and cisplatin on day 8. Blood pressure and ECG measurements were taken before sacrifice. Blood, liver, kidney, and heart samples were analyzed for oxidative stress markers, antioxidant enzyme activities, hematological, liver, and renal function indices. Cisplatin administration significantly elevated systolic blood pressure and markers of oxidative stress, while reducing antioxidant enzyme levels in cardiac and renal tissues. Treatment with FE and GA significantly reduced oxidative stress and restored antioxidant enzyme levels. The 200 mg/kg dose of Ficus exasperata showed the most pronounced protective effect. FE and GA exert protective effects against cisplatin-induced cardio-renal toxicity in rats, likely through antioxidant activity. The protective effect of Ficus exasperata appears dose-dependent.Item L-arginine and lisinopril supplementation protect against sodium fluoride-induced nephrotoxicity and hypertension by suppressing mineralocorticoid receptor and angiotensin-converting enzyme 3 activity(Springer Nature, 2023) Esan, O. O.; Maikifi, A. A.; Esuola, L. O.; Ajibade, T. O.; Adetona, M. O.; Aina, O. O.; Oyagbemi, A. A.; Adejumobi, O. A.; Omobowale, T. O.; Oladele, O. A.; Oguntibeju, O. O.; Nwulia, E.; Yakubu, M. A.Sodium fluoride (NaF) is one of the neglected environmental toxicants that has continued to silently cause toxicity to both humans and animals. NaF is universally present in water, soil and the atmosphere. The persistent and alarming rate of increase in cardiovascular and renal diseases and disorders caused by chemicals such as sodium fluoride (NaF) in mammalian tissues have led to the use of various drugs for the treatment of these diseases. This study aims at evaluating the renoprotective and antihypertensive effects of L- Arginine on NaF-induced nephrotoxicity. Thirty male Wistar rats (150–180 g) were used in this study. The rats were randomly divided into five groups of six rats each as Control, NaF (300 ppm), NaF + L- Arginine (100 mg/kg), NaF + L- Arginine (200 mg/kg), and NaF + Lisinopril (10 mg/kg), respectively; orally for eight days. Histopathological examination and immunohistochemistry of renal angiotensin converting enzyme (ACE) and mineralocorticoid receptor (MCR) were performed. Markers of renal damage, oxidative stress, antioxidant defence system, and blood pressure parameters were determined. L- Arginine significantly (p < 0.05) ameliorated the hypertensive effects of NaF. The systolic, diastolic and mean arterial blood pressure of the treated groups were significantly (p < 0.05) reduced compared with the hypertensive group. This finding was concurrent with significantly increased serum bioavailability of nitric oxide in the hypertensive treated groups. Also, there was significant reduction in the level of blood urea nitrogen (BUN) and creatinine in the serum of the hypertensive rats treated with L- arginine. There was significant (p < 0.05) reduction in markers of oxidative stress such as hydrogen peroxide (H2O2), malondialdehyde (MDA) and protein carbonyl (PCO) and concurrent increase in the levels of antioxidant enzymes in the kidney of hypertensive rats treated with L- arginine. The results of this study suggest that L- Arginine normalized high blood pressure, reduced oxidative stress, reduced the expression of renal ACE and MCR, and improved nitric oxide production. Thus, L- Arginine holds promise as a potential therapy against hypertension and renal damage.Item D-ribose-L-cystein prevents oxidative stress and cardiometabolic syndrome in high-fructose, high-fat-fed rats(Elsevier, 2021) Ojetola, A. A.; Adeyemi, W. J.; David, U. E.; Ajibade, T. O.; Adejumobi, O. A.; Omobowale, T. O.; Oyagbemi, A. A.; Fasanmade, A. A.Cardiometabolic syndrome has been linked with dietary modification. Therefore, we investigated the effects of D-ribose L cysteine (DRLC) in rats fed with high fructose high fat (IFF) diet. Twenty rats (n 5), divided into 4 groups were concurrently exposed to IIFIIF and/or DRLC (250 mg/kg, p.o) during the 8 weeks study. The result showed that compared to control group, HFHF group had significant impairment in lipid and glucose homeo- stasis, increased cardiac xanthine oxidase, systolic blood pressure, heart rate, body weight change and fluid intake. Also, there were significant reductions in HDL-C, cardiac (GPX, NO&GGT), feel intake and relative heart weight in the latter, relative to the former. However, there were no significant differences in most of the observed physical and biochemical changes in IIFIIF DRLC group compared to control. DRLC alone did not disrupt the level of biomarkers. Conclusively, DRLC prevented the manifestation of oxidative stress and cardiometabolic syndrome in IIFIIF diet fed rats.Item 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.Item 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.Item 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.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 Effect of Arsenic Acid Withdrawal on Hepatoxicity and Disruptor of Erythrocyte Antioxidant Defense System(Elsevier B.V, 2017) Oyagbemi, A. A.; Omobowale, T. O.; Adenuga, E. R.; Afolabi, J. M.; Adejumobi, O. A.; Adedapo, A. A.; Yakubu, M. A.We investigated the effects of withdrawal from Sodium arsenite (NaAsO2) on the hepatic and antioxidant defense system in male Wistar rats using a before and after texicant design. Rats were orally gavaged daily with varying duses of NaAsO fur a period of 4 weeks. One half of the population was sacrificed and the remaining half had the toxicant withdrawn for anodier ferther 4 weeks. Biochemical and immunohistochemical techniques were used to assess the impact of withdrawal on the erythrocyte and hepatic systems. Exposure of Wistar rats to NaASO, led to a significant (p<0.05) increase in hepatic and erythrocyte markers of oxidative stress (malondialdehyde, thiol contents and hydrogen peroxide generation). Concurrently, there was a significant (p < 0.05) increase in hepatic and erythrocyte antioxidant enzymes (glutathione-S-transferase, glutathione peroxidase and superoxide dismutase) following exposure. Withdrawal from NaAsO exposure led to a decline in both erythrocyte and hepatic markers of oxidative stress and together with a significant improvement in antioxidant defense system. Histopathology and immunohistochemistry revealed varying degrees of recovery in hepatocyte ultrastructure alongside increased expression of the pre-survival protein Kinase B (Akt/PKB) after 4 weeks of NAO with drawal. Conclusively, withdrawal from exposure led to a partial recovery from uxidative stress-mediated he patotoxicity and derangements in erythrocyte antioxidant system through Akt/PKB pathway.Item Ameliorative Effect of Azadirachta Indica on Sodium Fluoride-Induced Hypertension Through Improvement of Antioxidant Defence System and Upregulation of Extracellular Signal Regulated Kinase 1/2 Signaling(Walter de Gruyter GmbH (Berlin/Boston), 2017) Omóbòwálé, T. O.; Oyagbemi, A. A.; Alaba, B. A.; Ola-Davies, O. E.; Adejumobi, O. A.; Asenuga, E. R.; Ajibade, T. O.; Adedapo, A. A.; Yakubu, M. A.Background: Toxicities due to fluoride exposure from natural and industrial sources occur commonly in man and animals with severe consequences ranging from mild cardiac derangements to sudden death. In this study, we investigated the protective effects of the methanol extract of Azadirachta indica against sodium fluoride (NaF)-induced hypertension and genotoxicity in rats. Methods: Sixty rats were divided into six groups of ten rats each as follows: Group A, the control group received distilled water; Group B rats were administered NaF at 600 ppm in drinking water; Groups C and D rats were pre-treated with the methanol extract of AI and thereafter administered NaF at 600 ppm in drinking water for 7 consecutive days; Groups E and F rats were co-administered with AI and NaF. Results: The administration of NaF caused significant (p < 0.05) increases in the blood pressure, markers of oxidative stress, serum myeloperoxidase, xanthine oxidase values in NaF-alone treated rats, compared with the control. Significant (p < 0.05) decreases were observed in cardiac and renal antioxidant defence system in rats administered NaF alone compared with the control group. NaF treatment also resulted in a reduction in the expressions of extracellular signal-regulated kinase (ERK) 1/2 in cardiac and renal tissues of NaF-treated rats. Moreover, NaF treatment elicited an increase in the frequency of micronucleated polychromatic erythrocytes when compared with the control group. Conclusions: This study shows the protective effect of AI on NaF-induced hypertension and genotoxicity through antioxidant and ERK 1/2 signaling in rats.Item 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.