Scholarly works in Veterinary Surgery and Reproduction

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    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.
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    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.
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    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.
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    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.
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    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.
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    Luteolin normalizes Blood Pressure via its antioxidant activity and down-regulation of Renal Angiotensin II receptor and Mineralocorticoid receptor expressions in rats co-exposed to Diclofenac and Sodium Fluoride
    (Physiological Society of Nigeria, 2022) Ajibade, T. O.; Akinrinde, A. S.; Adetona, M. O.; Adedapo, A. D. A.; Oyagbemi, A. A.; Larbie, C.; Omobowale, T. O.; Ola-Davies, O. E.; Saba, A. B.; Adedapo, A. A.; Oguntibeju, O. O.; Yakubu, M. A.
    This study was designed to investigate the modulatory role of Luteolin (Lut), a flavonoid phytochemical, on haemodynamic parameters and the potential mechanisms involving renal Angiotensin II (AT2R) and Mineralocorticoid (MCR) receptors in renal toxicity induced by co-exposure to Diclofenac (Dcf) and sodium fluoride (NaF) in rats. Male Wistar rats were administered with either vehicle (control), Dcf only (9 mg/kg orally) or concurrently with NaF (300 ppm in drinking water). Other groups were treated with LutA (100 mg/kg) or LutB (200 mg/kg) along with Dcf and NaF exposures. All treatments lasted 8 days, following which blood pressure indices were measured using tail-cuff plethysmography. Renal expressions of AT2R and MCR were studied with immunohistochemistry, while biomarkers of oxidative and antioxidant status were also measured in the kidneys. Systolic, diastolic and mean arterial pressures were significantly (p<0.05) reduced in Dcf-treated rats, compared to control values. However, co-treatment with NaF or Lut restored these parameters. While the expression of AT2R and MCR was high in the Dcf and Dcf+NaF groups, treatment with Lut caused obvious reduction in the renal expression of these receptors. Increased lipid peroxidation (Malondialdehyde) and protein oxidation (protein carbonyls)with a lowering of reduced glutathione levels contributed to the renal toxicity of Dcf, and these were significantly ameliorated in Lut-treated rats. In conclusion, the preservation of haemodynamic indices by Luteolin in the experimental rats was probably mediated by mechanisms involving down-regulation of renal expressions of AT2R and MCR, reduction of oxidative stress and an improvement of renal antioxidant status.
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    Luteolin supplementation ameliorates cobalt-induced oxidative stress and inflammation by suppressing NF-кB/Kim-1 signaling in the heart and kidney of rats
    (Elsevier B.V., 2020) Oyagbemi, A. A.; Akinrinde, A. S.; Adebiyi, O. E.; Jarikre, T. A.; Omobowale, T. O.; Ola-Davies, O. E.; Saba, A. B.; Emikpe, B. O.; Adedapo, A. A.
    Cobalt-induced cardiomyopathy and renal toxicity have been reported in workers in processing plants, hard metal industries, diamond polishing and manufacture of ceramics. This study was designed to investigate the influence of Luteolin supplementation on cobalt-induced cardiac and renal toxicity in rats. Exposure of rats to cobalt chloride (CoCl2) alone caused significant (p < 0.05) increases in cardiac and renal H2O2, malondialdehyde (MDA) and nitric oxide (NO), along with increased serum myeloperoxidase (MPO) activity. In addition, there were significant (p < 0.05) reductions in cardiac and renal glutathione peroxidase (GPx), glutathione S-transferase (GST) and reduced glutathione (GSH). CoCl2 induced higher immuno-staining of nuclear factor kappa beta (NF-κB) in the heart and kidneys, and the kidney injury molecule (Kim-1) in the kidneys. Treatment with Luteolin or Gallic acid produced significant reversal of the oxidative stress parameters with reductions in NF-κB and Kim-1 expressions, leading to suppression of histopathological lesions observed in the tissues.
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    Fluoride‑induced hepatotoxicity is prevented by L‑Arginine supplementation via suppression of oxidative stress and stimulation of nitric oxide production in rats
    (Springer, 2021) Akinrinde, A. S.; Tijani, M.; Awodele, O. A.; Oyagbemi, A. A.
    Objective Concerns over fluoride toxicity have increased in recent times due to high exposures from various anthropogenic sources such as industrial sites, fluoride-containing pesticides, drugs, dental products, refridgerants and fire extinguishers. There is, therefore, continued search for agents that could ameliorate the toxicity of this chemical in various body organs. In this study, we sought to investigate the protective effects of L-Arginine (L-Arg), a nitric oxide donor, on liver toxicity induced by sodium fluoride (NaF) in rats. Methods Rats received NaF (300 mg L−1) in drinking water alone or in co-treatment with L-Arg at two different doses, 100 and 200 mg kg−1, by oral gavage, for 7 days. Markers of hepatotoxicity, oxidative stress and antioxidant status were thereafter assessed. Results NaF caused marked increase in serum transaminases: alanine aminotransferase, Aspartate aminotransferase and Alkaline phosphatase, along with atrophy of the centri-lobular hepatic cords and dilatation of the sinusoids. Moreover, NaF stimulated increases in hepatic contents of hydrogen peroxide (H2O2), nitric oxide (NO), protein carbonyls, malondialdehyde and advanced oxidation protein products. NaF also inhibited the activities of antioxidant enzymes, Glutathione peroxidase and Superoxide dismutase. However, L-Arg supplementation caused significant alleviation of NaF hepatotoxicity by reducing lipid and protein oxidation indices, stimulation of antioxidant systems along with increased production of NO. Conclusions L-Arg showed promise as a potential protective agent against NaF-induced hepatotoxicity via restoration of oxidant-antioxidant balance. Further studies are required to understand the involvement of NO signaling in the protective effects of L-Arg against fluoride toxicity.
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    Cobalt chloride-induced oxidant-antioxidant imbalance in rat erythrocytes: The modulatory role of Kolaviron
    (Faculty of Veterinary Medicine, University of Ibadan, Nigeria., 2018) Akinrinde, A. S.; Idowu, O. O.; Oyagbemi, A. A.; Omobowale, T. O.
    Cobalt stimulates erythrocyte production via mechanisms that mimic physiological adaptations to hypoxic conditions. However, little is known about alterations in the balance of erythrocyte antioxidant defense system produced by cobalt. We investigated the effect of Kolaviron (KV) on cobalt chloride (CoCl2)-induced disturbances in erythrocyte antioxidant status and hematological parameters and compared the effects with those of Gallic acid (GA). Groups of rats were orally treated with either KV1 (100 mg/kg), KV2 (200 mg/kg) or GA (120 mg/kg), along with CoCl2 (350 ppm) in drinking water for 14 days. CoCl, produced significant (p<0.05) increases in packed cell volume, hemoglobin and red blood cell count, but no alterations in erythrocyte morphology, in the same way as rats treated with KV or GA. Significant (p<0.05) elevation in malondialdehyde (MDA) content and reductions in total thiols and reduced glutathione (GSH) in the CoCl2 group were indications of oxidative stress. KV produced significant (p<0.05) reduction in MDA, while restoring the levels of GSH and total thiols with elevations in" glutathione S-transferase and superoxide dismutase. Our results indicate that CoCl2-induced erythropoiesis was accompanied by altered antioxidant status of the erythrocytes. Kolaviron, however, ameliorated the disturbancesin erythrocyte antioxidant defense system.
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    Phytochemical profiling, antioxidant activities and essential oil constituents of Andrographis paniculata
    (Faculty of Veterinary Medicine, University of Ibadan, Nigeria, 2018) Adesye, B. Q.; Akinrlnde, A. S.; Oyagbemi, A. A.; Omobowale, T. O.; Afofayan, A. J.; Adedapo, A. A.
    Oxidative stress is involved in the pathogenesis of various diseases which lead to urgent need to investigate new, safe and effective source of antioxidant agents. This research proposed to investigate in-vitro and phytochemical constituent of the plant Ancirographis paniculatei using phytochemical analysis, GC/MS, DPPH, ABTS, FRAP and NO. Phytochemical analysis of Anclrographis paniculata revealed the presence of tannins, total fiavonoids, total phenol, total flavonols, and total proanthocyanidins. GC/MS analysis of essential oil of AP identified one major compound name benzencpropanoic acid clucked at 3.296 retention time and 0.74 area percentage. The ferric reducing potential of the extracts was concentration dependent and significantly different from that of rutin and vitamin E. The% inhibition of ABTS by the ethanol leaf extract of Anclrographis paniculata was concentration dependent and compared favourably well with the rutin and vitamin E, in DPPH scavenging assays, the IC50 value of the ethanol leaf extract of Andrographis paniculata was < 0.025 mg/ml, while IC50 of rutin and Vitamin E were < 0.025 mg/ml and 0.68mg/ml. Nitric oxide IC50, for extract is 1,05mg/ml, Vitamin E is 1.2 mg/ml, and rutin is < 0.025 mg/ml. The present study showed high level of radical scavenging activity by ethanol leaf .extract of Andrographis paniculata with higher antioxidant activities than Vitamin E but less than that of rutin. This show that Andrographis paniculata has antioxidant properties and the plant epuid be used in the prevention and treatment of diseases associated with oxidative stress.