Veterinary Surgery & 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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    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.
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    Rutin and Melatonin ameliorate the gastrointestinal and hepatic injuries induced by oral Lead Acetate in rats
    (Arak University of Medical Sciences, 2023) Akinrinde, S. A.; Oladipo, O. O.; Adetiba, R.; Ademola, A. O.; Temidayo, O. O.
    Background: Oral ingestion of lead in drinking water represents the most common route of human and animal exposure, especially in the developing nations. Unlike other internal organs, research on the effects of lead on gastrointestinal tract remains limited. This study explored the alterations in faecal fatty acid composition, gastrointestinal and hepatic histologies and redox status, following chronic, 90-day exposure of rats to lead acetate (PbA). We also investigated the protective effects of rutin and melatonin against lead toxicity in rats. Methods: Fifty male Wistar rats were randomly divided into five groups of 10 (A-E) and were assigned as follows: A: Control; B: 1% PbA in drinking water; C: PbA+rutin (50 mg/kg); D: PbA+melatonin (25 mg/kg) and E: PbA+rutin+melatonin. The faecal fatty acid profiles were quantified by methylation and gas chromatography-flame ion detection. We also evaluated the oxidative stress and antioxidant markers for the stomach, liver, and guts, and their histopathological alterations. Results: Exposure to PbA caused remarkable elevations of the faecal fats, such as undecylic, lauric, tridecylic, myristic, and palmitic acids, compared to the controls and rats in group C. The administration of rutin and/or melatonin ameliorated the PbA-induced increases in the hydrogen peroxide and malondialdehyde contents. Rutin and melatonin improved the levels of thiol, and reduced the glutathione, glutathione S-transferase and superoxide dismutase activities. Conclusion: The findings suggest that rutin alone or combined with melatonin protects against PbA-induced disruption of the liver and gastrointestinal tract integrity via modulation of intestinal total lipids in cells and redox imbalances.
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    Cobalt-induced neuro-behavioural alterations are accompanied by profound Purkinje cell and gut-associated responses in rats
    (The Korean Society of Environmental Health and Toxicology, 2023) Akinrinde, A.; Adigun, K.; Mustapha, O.
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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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    The International Natural Product Sciences Taskforce (INPST) and the power of Twitter networking exemplified through #INPST hashtag analysis
    (Elsevier GmbH, 2023) Singla, R. K.; De, R.; Efferth, T.; Mezzetti, B.; Uddin, M. S.; Sanusi, S.; Ntie-Kang, F.; Wang, D.; Schultz, F.; Kharat, K. R.; Devkota, H. P.; Battino, M.; Sur, D.; Akinrinde, A. S.
    Background: The development of digital technologies and the evolution of open innovation approaches have enabled the creation of diverse virtual organizations and enterprises coordinating their activities primarily on-line. The open innovation platform titled “International Natural Product Sciences Taskforce” (INPST) was established in 2018, to bring together in collaborative environment individuals and organizations interested in natural product scientific research, and to empower their interactions by using digital communication tools. Methods: In this work, we present a general overview of INPST activities and showcase the specific use of Twitter as a powerful networking tool that was used to host a one-week “2021 INPST Twitter Networking Event” (spanning from 31st May 2021 to 6th June 2021) based on the application of the Twitter hashtag #INPST. Results and Conclusion: The use of this hashtag during the networking event period was analyzed with Symplur Signals (https://www.symplur.com/), revealing a total of 6,036 tweets, shared by 686 users, which generated a total of 65,004,773 impressions (views of the respective tweets). This networking event’s achieved high visibility and participation rate showcases a convincing example of how this social media platform can be used as a highly effective tool to host virtual Twitter-based international biomedical research events.
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    Supplementation with sesame oil suppresses genotoxicity, hepatotoxicity and enterotoxicity induced by sodium arsenite in rats
    (BioMed Central, 2023) Akinrinde, A. S.; Oyewole, S. O.; Ola-Davies, O. E.
    Background Sesame oil, an edible essential oil, is known to be rich in unsaturated fatty acids, vitamins and lignans with several reported health-promoting benefts. Acute arsenic poisoning produces toxic hepatitis, bone marrow depression and adverse gastrointestinal responses. In this study, we investigated the protective efect of sesame seed oil (SSO) against genotoxicity, hepatotoxicity and colonic toxicity induced by sodium arsenite (SA) in Wistar rats. Methods Twenty-eight male Wistar albino rats were randomly allocated into four groups: control, SA only (2.5 mg/ kg), SA + SSO (4 ml/kg) and SSO alone for eight consecutive days. Liver function and morphology, bone marrow micronuclei induction, colonic histopathology, mucus production and immune expression of Bcl-2, carcinoembryonic antigen (CEA), MUC1 and cytokeratins AE1/AE3 were evaluated. Results SA provoked increased serum activities of liver enzymes, including alanine aminotransferase (ALT) and aspar tate aminotransferase (AST), and caused severely altered morphology of hepatic and colonic tissues with increased frequency of micronucleated polychromatic erythrocytes (MnPCEs/1000PCE) in the bone marrow. In addition, SA triggered increased expression of colonic CEA and MUC1 but weak Bcl-2 immunoexpression. However, cotreatment with SSO demonstrated protective activities against SA-induced damage, as indicated by signifcantly reduced serum ALT and AST, fewer micronucleated bone marrow erythrocytes and well-preserved hepatic and colonic morphologies compared to the SA-treated rats. Furthermore, SSO protected the colonic mucosa by boosting mucus production, elevating anti-apoptotic Bcl-2 expression and reducing CEA expression. GC–MS analysis of SSO revealed that it was predominated by linoleic acid, an omega-3 fatty acid, and tocopherols. Conclusions Our data indicated that SSO protected the liver, colon and bone marrow potentially via anti-infam matory and anti-apoptotic activities. The data suggest that sesame oil has potential therapeutic applications against chemical toxicities induced by arsenic.
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    Infuence of zinc and gallic acid on haematological alterations, hepatic and intestinal toxicity induced by sub‑acute exposure to Dibutyl‑n‑phthalate (DBP) in Wistar rats
    (Springer Nature Link, 2022) Akinrinde, A. S.; Bello, A. V.; Soetan, K. O.
    Objective Dibutyl-n-phthalate (DBP) is utilized industrially as a plasticizer, as well as in consumer products, food processing and medical applications, but there are concerns over its safety. This study investigated the protective effect of Zinc sulphate (Zn) and Gallic acid (GA) against haematological, hepatic and intestinal alterations following sub-acute (14-day) DBP exposure in rats. Methods Twenty-four male Wistar rats weighing 150–190g were randomly allocated into 4 groups (n=6). Group A (Control) received normal saline at 2 ml/kg. Group B was given DBP (500 mg/kg bw/day) by oral gavage for 14 days. Groups C and D were treated concurrently with Zn (250 mg/kg bw) and GA (120 mg/kg bw), respectively, in addition to DBP treatment. Results Administration of DBP resulted in significant (p<0.05) elevation of serum Alanine transmainase and alkaline phosphatatse, signifcant (p<0.05) increase in faecal counts of coliforms and Escherichia coli (Proteobacteria), as well as reduced colonic mucus production and goblet cell numbers. Histological evidence of DBP toxicity included severe congestion of hepatic central venules, severe infammatory cell infltration in liver and colonic tissues, and atrophy of colonic mucosal glands, with a reduction in erythrocyte count being the major haematological alteration. The protective efects of Zn and GA were manifested as signifcant reduction in the activities of serum enzymes and the severity of hepatic and colonic lesions, along with preservation of haematological indices and colonic mucus. GA caused signifcant reduction in E. coli and coli forms, while also increasing enterococci count. Conclusion Dietary supplementation with Zn or GA may alleviate DBP-induced liver and colonic toxicity. The probable mechanisms may include the preservation of the colonic mucus barrier and improvement in the abundance of beneficial bacteria.