Scholarly works in Veterinary Surgery and Reproduction
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Item Glycine exerts renal antioxidant effects and restores hemodynamic alterations in Rats treated with Diclofenac Sodium: Roles of renal Angiotensin Converting Enzyme, Angiotensin II Receptor and Mineralocortocoid Receptor(Biomedical Communications Group, Ibadan, 2023) Akinrinde, A. S.; Ajibade, T. O.; Adetona, M. O.; Oyagbemi, A. A.; Adedapo, A. D. A.; Larbie, C.; Omobowale, T. O.; Ola-Davies, O. E.; Adedapo, A. A.; Saba, A. B.; Oguntibeju, O. O.; Yakubu, M. A.Diclofenac (DIC) is known to alter renal function in the form of hemodynamically-mediated acute renal failure. This study evaluated the protective role of the amino acid, glycine (Gly) on nephrotoxicity and acute hemodynamic alterations induced by DIC (9 mg/kg) in male Wistar rats. The rats were divided into four groups (n=7/group) including Group A (control); Group B (DIC-treated), Groups C (DIC + Gly1, 250 mg/kg) and Group D (DIC + Gly2 500 mg/kg). Systolic (SBP), diastolic (DBP) and mean arterial (MAP) blood pressures were significantly (p<0.05) reduced in rats treated with DIC alone, compared to control. Kidneys from DIC-treated rats showed altered histology with significantly (p<0.05) increased hydrogen peroxide (H2O2), malondialdehyde (MDA) and protein carbonyl contents, but decreased glutathione (GSH) glutathione peroxidase (GPx), glutathione S-transferase (GST) and superoxide dismutase (SOD) activities. Immunohistochemistry revealed down-regulation of renal angiotensin converting enzyme (ACE), but increased expressions of angiotensin type II receptor (AT2R) and mineralocorticoid receptor (MR) in DIC-treated rats. However, pre-treatment with Gly reversed most of the aforementioned effects of DIC. The present results suggest that oral glycine protected kidney tissues and restored DIC-induced hemodynamic changes by modifying renal expression of the renin-angiotensin-mineralocortocoid pathway and/or renal oxidative stress.Item Glycine exerts renal antioxidant effects and restores hemodynamic alterations in Rats treated with Diclofenac Sodium: Roles of renal Angiotensin Converting Enzyme, Angiotensin II Receptor and Mineralocortocoid Receptor(Biomedical Communications Group, Ibadan, 2023) Akinrinde, A. S.; Ajibade, T. O.; Adetona, M. O.; Oyagbemi, A. A.; Adedapo, A. D. A.; Larbie, C.; Omobowale, T. O.; Ola-Davies, O. E.; Adedapo, A. A.; Saba, A. B.; Oguntibeju, O. O.; Yakubu, M. A.Diclofenac (DIC) is known to alter renal function in the form of hemodynamically-mediated acute renal failure. This study evaluated the protective role of the amino acid, glycine (Gly) on nephrotoxicity and acute hemodynamic alterations induced by DIC (9 mg/kg) in male Wistar rats. The rats were divided into four groups (n=7/group) including Group A (control); Group B (DIC-treated), Groups C (DIC + Gly1, 250 mg/kg) and Group D (DIC + Gly2 500 mg/kg). Systolic (SBP), diastolic (DBP) and mean arterial (MAP) blood pressures were significantly (p<0.05) reduced in rats treated with DIC alone, compared to control. Kidneys from DIC-treated rats showed altered histology with significantly (p<0.05) increased hydrogen peroxide (H2O2), malondialdehyde (MDA) and protein carbonyl contents, but decreased glutathione (GSH) glutathione peroxidase (GPx), glutathione S-transferase (GST) and superoxide dismutase (SOD) activities. Immunohistochemistry revealed down-regulation of renal angiotensin converting enzyme (ACE), but increased expressions of angiotensin type II receptor (AT2R) and mineralocorticoid receptor (MR) in DIC-treated rats. However, pre-treatment with Gly reversed most of the aforementioned effects of DIC. The present results suggest that oral glycine protected kidney tissues and restored DIC-induced hemodynamic changes by modifying renal expression of the renin-angiotensin-mineralocortocoid pathway and/or renal oxidative stress.Item Glycine exerts renal antioxidant effects and restores hemodynamic alterations in Rats treated with Diclofenac Sodium: Roles of renal Angiotensin Converting Enzyme, Angiotensin II Receptor and Mineralocortocoid Receptor(Biomedical Communications Group, Ibadan, 2023) Akinrinde, A. S.; Ajibade, T. O.; Adetona, M. O.; Oyagbemi, A. A.; Adedapo, A. D. A.; Larbie, C.; Omobowale, T. O.; Ola-Davies, O. E.; Adedapo, A. A.; Saba, A. B.; Oguntibeju, O. O.; Yakubu, M. A.Diclofenac (DIC) is known to alter renal function in the form of hemodynamically-mediated acute renal failure. This study evaluated the protective role of the amino acid, glycine (Gly) on nephrotoxicity and acute hemodynamic alterations induced by DIC (9 mg/kg) in male Wistar rats. The rats were divided into four groups (n=7/group) including Group A (control); Group B (DIC-treated), Groups C (DIC + Gly1, 250 mg/kg) and Group D (DIC + Gly2 500 mg/kg). Systolic (SBP), diastolic (DBP) and mean arterial (MAP) blood pressures were significantly (p<0.05) reduced in rats treated with DIC alone, compared to control. Kidneys from DIC-treated rats showed altered histology with significantly (p<0.05) increased hydrogen peroxide (H2O2), malondialdehyde (MDA) and protein carbonyl contents, but decreased glutathione (GSH) glutathione peroxidase (GPx), glutathione S-transferase (GST) and superoxide dismutase (SOD) activities. Immunohistochemistry revealed down-regulation of renal angiotensin converting enzyme (ACE), but increased expressions of angiotensin type II receptor (AT2R) and mineralocorticoid receptor (MR) in DIC-treated rats. However, pre-treatment with Gly reversed most of the aforementioned effects of DIC. The present results suggest that oral glycine protected kidney tissues and restored DIC-induced hemodynamic changes by modifying renal expression of the renin-angiotensin-mineralocortocoid pathway and/or renal oxidative stress.Item Protective effect of cholecalciferol against cobalt‑induced neurotoxicity in rats: ZO‑1/iFABP, ChAT/AchE and antioxidant pathways as potential therapeutic targets(Springer Science+Business Media, LLC, 2024) Akinrinde, A. S.; Adeoye, B. O.; Samuel, E. S.; Mustapha, O. A.Cobalt (Co) toxicity has been reported to produce central nervous system and gastrointestinal abnormalities. This study assessed the therapeutic effect of cholecalciferol (Cho) supplementation against damages caused by sub-acute (14-day) cobalt chloride (CoCl2) exposure in the brain and intestines. Thirty-five male Wistar rats were divided equally into five groups: Group I (control) received no treatment; Group II received oral CoCl2 (100 mg/kg) only; Groups III, IV, and V received 1000, 3000 and 6000 IU/kg of cholecalciferol, respectively by oral gavage, and concurrently with CoCl2. Cobalt-treated rats showed neuronal vacuolation and presence of pyknotic nuclei in the cerebral cortex and hippocampus, depletion of Purkinje cells in the cerebellum, as well as inflammation and congestion in the intestinal mucosa. Cobalt also increased brain and intestinal hydrogen peroxide (H2O2) and malondialdehyde (MDA) concentrations, while simultaneously reducing glutathione (GSH) content, superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione S-transferase (GST) activities. Further, CoCl2 induced increases in brain acetylcholinesterase (AchE) activity and serum zonulin (ZO-1) levels. Conversely, Cho administration suppressed CoCl2-induced damages in the brain and intestines by reducing lipid peroxidation and increasing the activities of antioxidant enzymes. Remarkably, Cho produced stimulation of brain choline acetyltransferase (ChAT) and suppression of AchE activity, along with dose-dependent reduction in serum levels of ZO-1, intestinal fatty acid-binding protein (iFABP) and nitric oxide. In conclusion, the protective role of cholecalciferol against cobalt-induced toxicity occurred via modulation of cholinergic, intestinal permeability and antioxidant pathways. The results may prove significant in the context of the role of gut-brain connections in neuroprotection.Item Dose‑dependent effects of cobalt chloride supplementation in a rat model of acetic acid‑induced ulcerative colitis(Springer-Verlag London Ltd., 2024) Akinrinde, A. S.; Samuel, E. S.; Adeoye, B. O.Several recent studies have shown that hypoxia preconditioning, often mimicked by sub-toxic levels of cobalt, can protect body tissues against various types of inflammatory and oxidative injuries. The present study was designed to understand the effects of low-to-moderate doses of cobalt chloride (CoCl2) on ulcerative colitis induced by acetic acid in male Wistar rats. Rats were pre-treated with CoCl2 at 10, 30 and 60 mg/kg BW for 7 days prior to, and later along with intra-rectal administration of 4% acetic acid for another 3 days. Rats were euthanized and the colons were examined macroscopically, and histologically, haematological parameters were evaluated in the blood and various oxidative stress parameters and inflammatory cytokines were studied in the colon and blood. Pre-treatment with CoCl2 at 10 mg/kg caused reduction in colonic levels of hydrogen peroxide (H2O2), nitric oxide (NO), advanced oxidation protein products (AOPP) and reduced serum TNF-α, but increased serum IL-10 levels. Conversely, rats treated with higher doses of CoCl2 showed exacerbation of macroscopic scores and histologic damage in the colon, with significantly elevated levels of oxidants and serum TNF-α along with reduced serum IL-10 levels. Values of all the measured haematological parameters (PCV, Hb, RBC, WBC and platelet count) were dose-dependently increased with increasing doses of CoCl2. The results of this study showed that consumption of cobalt at low doses could play a vital role in the control of ulcerative colitis, while higher doses can contribute to exacerbation of intestinal inflammation. Monitoring of cobalt concentrations in food and water consumed by ulcerative colitis patients is imperative to prevent exacerbation of colonic inflammation by cobalt.Item Protective effect of cholecalciferol against cobalt‑induced neurotoxicity in rats: ZO‑1/iFABP, ChAT/AchE and antioxidant pathways as potential therapeutic targets(Springer Science+Business Media, LLC, 2024) Akinrinde, A. S.; Adeoye, B. O.; Samuel, E. S.; Mustapha, O. A.Cobalt (Co) toxicity has been reported to produce central nervous system and gastrointestinal abnormalities. This study assessed the therapeutic effect of cholecalciferol (Cho) supplementation against damages caused by sub-acute (14-day) cobalt chloride (CoCl2) exposure in the brain and intestines. Thirty-five male Wistar rats were divided equally into five groups: Group I (control) received no treatment; Group II received oral CoCl2 (100 mg/kg) only; Groups III, IV, and V received 1000, 3000 and 6000 IU/kg of cholecalciferol, respectively by oral gavage, and concurrently with CoCl2. Cobalt-treated rats showed neuronal vacuolation and presence of pyknotic nuclei in the cerebral cortex and hippocampus, depletion of Purkinje cells in the cerebellum, as well as inflammation and congestion in the intestinal mucosa. Cobalt also increased brain and intestinal hydrogen peroxide (H2O2) and malondialdehyde (MDA) concentrations, while simultaneously reducing glutathione (GSH) content, superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione S-transferase (GST) activities. Further, CoCl2 induced increases in brain acetylcholinesterase (AchE) activity and serum zonulin (ZO-1) levels. Conversely, Cho administration suppressed CoCl2-induced damages in the brain and intestines by reducing lipid peroxidation and increasing the activities of antioxidant enzymes. Remarkably, Cho produced stimulation of brain choline acetyltransferase (ChAT) and suppression of AchE activity, along with dose-dependent reduction in serum levels of ZO-1, intestinal fatty acid-binding protein (iFABP) and nitric oxide. In conclusion, the protective role of cholecalciferol against cobalt-induced toxicity occurred via modulation of cholinergic, intestinal permeability and antioxidant pathways. The results may prove significant in the context of the role of gut-brain connections in neuroprotection.Item Taurine and protocatechuic acid attenuate Vincristine sulphate‑induced bone marrow, liver and intestinal injuries via anti‑oxidative, anti‑inflammatory and anti‑apoptotic activities(Springer Nature, 2024) Akinrinde, A. S.; Ajao, J. J.; Oyagbemi, A. A.; Ola-Davies, O. E.Chemotherapy with Vincristine (Vcr) is often compromised by undesirable gastrointestinal, myeloid and hepatic effects. In this study, we evaluated and compared the efficacy of taurine (Tau) and/or protocatechuic acid (Pca) in alleviating Vcr-induced hepatotoxicity, enterotoxicity and myelotoxicity in rats. In two cycles of five daily injections each, rats were exposed to Vcr (0.1 mg/kg, i.p.) alone or in combination with orally administered Tau (50 mg/kg) and/or Pca (50 mg/kg). Blood was collected for haematology and measurement of liver enzymes and inflammatory cytokines. Genotoxicity assay was performed on bone marrow, while the liver and intestines were subjected to biochemical assays, histopathology and immunohisto-chemical staining. Administration of Vcr triggered bone marrow suppression (anaemia, leucopenia, thrombocytopenia and increased frequency of micronucleated polychromatic erythrocytes, MnPCEs), increased serum transaminases (ALT, AST) and alkaline phosphatase (ALP) and altered hepatic and intestinal morphology. However, supplementation with Tau and/ or Pca alleviated most of the toxic effects of Vcr by reducing tissue levels of malondialdehyde (MDA), hydrogen peroxide (H2O2) and advanced oxidation protein products (AOPP), but stimulating glutathione S-transferase (GST) and glutathione per oxidase (GPx) activities. In addition, Tau and/or Pca enhanced anti-inflammatory (reduced serum TNFα) and anti-apoptotic mechanisms (reduced cytochrome c/Bax expression and increased Bcl-2 expression) in the ileum and liver. Overall, Tau or Pca protected the liver, ileum and bone marrow against Vcr-induced toxicities via antioxidant, anti-inflammatory and anti-apoptotic mechanisms. The data supports their individual use, rather than their combination, as adjuvant therapy in patients undergoing chemotherapeutic intervention.Item Terpenoid profiles of the essential oils from the underground parts of Dianthus thunbergii S.S. Hooper and Hypoxis argentea Harv ex Baker as affected by pre-distillation drying(International Academy of Ecology and Environmental Sciences, 2024) Akinrinde, A. S.; Afolayan, A. J.; Bradley, G.The roots of Dianthus thunbergii and corms of Hypoxis argentea are commonly used in the Eastern Cape Province of South Africa for various medicinal purposes, although their effectiveness as fresh or dried forms is often a subject of debate. The compositions of the volatile oils from the underground parts of these plants were analyzed for the first time by gas chromatography-mass spectrometry (GC-MS). The yields of the essential oil fractions from fresh and oven-dried plant parts varied from 0.42-0.72%. The terpenoid composition of D. thunbergii oils were dominated by α-pinene and β-selinene, although overall terpenoid content decreased from 77.17% in fresh roots to 47.58% in the dried roots. H. argentea corm oils were dominated by alkanes, amides and amino acids, while total terpenoid content of the oils from fresh and dried corms were 10.85% and 3.45%, respectively. Generally, pre-distillation drying of the underground parts of both plants produced significant reductions in the terpenoid composition of the volatile oils, suggesting that drying may considerably reduce their medicinal potentials.Item Evaluation of the Effects of Alpha Evaluation of the effects of Alpha Tocopherol, Quercetin and their combination on Ethanol-Induced pancreatic and duodenal mucosal injuries: An experimental study.(Sciencedomain International, 2024) Akinrinde, A. S.; Ajibade, T. O.Aim: In this study, the effects of alpha-tocopherol (AT), quercetin (QT) or their combination on ethanol-induced pancreatic and duodenal mucosal damage were investigated in rats using morphological and biochemical evaluations. Study Design: Experimental study.Place and Duration of Study: University of Ibadan, Ibadan, Nigeria. Methodology: Ethanol-induced injuries were produced by oral administration of 40% ethanol (0.2 ml/day) for 40 consecutive days, while a control group of rats was served distilled water. Other groups received AT (2.5 mg/kg), QT (50 mg/kg) or their combination with 40% ethanol during the experimental period. Blood glucose level was significantly (p<0.05) increased in ethanol-treated rats relative to controls. Ethanol administration caused shrinkage of insulin-secreting islets tissues in the pancreas, while lesions such as erosions, loss of villi and severe inflammatory cell infiltrations of the mucosa and sub-mucosa were observed in the duodenum. These changes were accompanied by significant elevation in the levels of hydrogen peroxide (H2O2), malondialdehyde (MDA) and advanced oxidation protein products (AOPP) in the pancreas and duodenum, along with reduced activities of glutathione peroxidase (GPx) and glutathione S-transferase (GST). Treatment of rats with AT, QT, and especially their combination, yielded profound reversal of ethanol-induced effects indicated by restoration of blood glucose to control levels, preservation of pancreatic and duodenal morphology and the inhibition of ethanol-induced oxidative stress. Conclusion: Overall, dietary supplementation with AT and/or QT could potentially counteract the adverse effects associated with chronic alcohol consumption.Item Argania spinosa essential oil ameliorates colonic damage and extraintestinal alterations in a rat model of acetic acid‑induced colitis by suppressing oxidative stress and inflammation(Springer Nature, 2023) Olojo, F. O.; Akinrinde, A. S.; Ogundairo, S. A.; Ubochi, V. C.The present study was designed to elucidate the prophylactic and therapeutic potential of argan oil (AO) (from the kernels of the argan tree, Argania spinosa) against acetic acid (AA)-induced colitis and associated alterations in the liver and kidneys of rats. Colitis was induced by intra-rectal administration of 4% AA solution for 3 consecutive days. Some groups of rats were treated orally with AO (5 mL/kg) for 5 consecutive days before and after AA administration, while other groups were treated with either the vehicle or AO alone. Macroscopic and microscopic lesions in the tissues were assessed, while oxidative stress, antioxidant parameters and myeloperoxidase (MPO) activity were determined by biochemical methods. Haematological and serum chemistry parameters were also evaluated. Administration of AO before or after AA induction produced improvements in body weight gain, faecal consistency, macroscopic and histologic scores of the colonic mucosa compared to rats treated with AA alone. Furthermore, AO treatment caused significant reduction in colonic levels of hydrogen peroxide (H2O2), malondialdehyde (MDA), advanced oxidation protein products (AOPP) and serum MPO activity, while glutathione S-transferase (GST) and superoxide dismutase (SOD) activities were increased in the colon and kidneys, compared to the colitis control. Acetic acid treatment resulted in significant reduction in erythrocyte and leucocyte indices in relation to healthy controls. Taken together, treatment of rats with AO protected colonic tissues from acetic acid-induced inflammation and suggests that the oil may be considered for preventive and therapeutic purposes against inflammatory bowel diseases.