Scholarly works in Veterinary Surgery and Reproduction
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Item Amelioration of Aflatoxin B1-induced gastrointestinal injuries by Eucalyptus oil in rats(Walter de Gruyter GmbH, 2019) Akinrinde, A. S.; Adebiyi, O. E.; Asekun, A.Background: Eucalyptus oil (EO), derived from Eucalyptus species, possesses vast remedial and healing properties, although its gut health-promoting properties have not been well investigated. In this study, we investigated the chemical composition of a commercial EO formulation and its potential role in protecting against aflatoxinmB1 (AfB1)-induced gastrointestinal damage in rats. Methods: Male Wistar rats were divided into six groups with eight rats each. Control rats were administered with the vehicle (1% Tween 80) for 14 days, while another group was exposed to two oral doses of AFB1 on days 12 and 14. Two other groups were pre-treated with oral doses of EO (50 and 100 mg/kg b.w.) for 14 consecutivedays, along with two oral doses of AfB1 (5 mg/kg b.w.) on days 12 and 14. The remaining two groups weretreated with EO alone at the two doses for 14 days. At the end of the experiment, blood samples, stomachand intestinal tissues were collected for measurement of oxidative stress and antioxidant parameters and lightmicroscopic examination. Results: Gas chromatography-mass spectrometry analysis revealed Eucalyptol (1, 8-cineole) as the main con stituent (67.48%) of the oil. AfB1 administration induced oxidative and inflammatory disturbances, indicated by significantly (p<0.05) increased serum nitric oxide level and myeloperoxidase activity; increased tissue contents of hydrogen peroxide, malondialdehyde and protein carbonyls, accompanied with corresponding histological alterations. AfB1 also induced significant (p<0.05) reductions in glutathione peroxidase and superoxide dismutase (SOD) activities. Treatment with EO produced significant improvements in the biochemical parameters as well as the appearance of the gastric and intestinal mucosa. EO alone, at the two doses tested did not produce any significant changes in the parameters investigated. Conclusion: The findings from this study showed that EO demonstrated protective activity against Aflatoxin induced toxicity in stomach and intestinal tissues and may thus find application in treatment of gastrointestinal disorders.Item Neuroprotection by luteolin and gallic acid against cobalt chloride-induced behavioural, morphological and neurochemical alterations in Wistar rats(Elsevier B.V., 2019) Akinrinde, A. S.; Adebiyi, O. E.Cobalt (Co) intoxication arising from occupational exposures and ion release from metal implants has been associated with neurological alterations such as cognitive decline, incoordination and depression. The present study evaluated the mechanisms of neuro-protection exerted by Luteolin (Lut; 100 mg/kg) and Gallic acid (GA; 120 mg/kg) in Wistar rats exposed to cobalt chloride (CoCl2) at 150 mg/kg for 7 consecutive days. Results indicate that CoCl2 induced neuro-behavioural deficits specifically by decreasing exploratory activities of CoCl2- exposed rats, increased anxiety, as well as significant reduction in hanging latency. Co-treatment with Lut or GA, however, restored these parameters to values near those of normal controls. Moreover, Lut and GA prevented CoCl2-induced increases in hydrogen peroxide (H2O2), malondialdehyde (MDA) and nitric oxide (NO) in the brain, while also restoring the activities of acetylcholinesterase, glutathione S-transferase (GST) and superoxide dismutase (SOD). In addition, Lut and GA produced significant reversal of CoCl2-induced elevation in levels of serum Interleukin 1 beta (IL-1β) and Tumor necrosis factor (TNFα). Meanwhile, immunohistochemistry revealed increased astrocytic expression of glial fibrillary acidic protein (GFAP), with intense calbindin (CB) D-28k staining and pronounced dendrites in the Purkinje cells. In contrast, the CoCl2 group was characterized by decreased number of neurons expressing CB and dendritic loss. Taken together, mechanisms of luteolin and/or gallic acid protection against Co toxicity involved restoration of Ca2+ homeostasis, acetylcholinesterase and antioxidant enzyme activities, as well as inhibition of lipid peroxidation in the brain.Item 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.Item Phytochemical, analgesic, in-vitro anti-oxidant and GC-MS analysis of Vernonia amygdalina leaves(Ibadan Biomedical Communications Group, 2018) Adeoye, A. T.; Akinrinde, A. S.; Oyagbemi, A. A.; Omobowale, T. O.; Adedapo, A. D. A.; Ayodele, E. A.; Yakubu, M. A.; Adedapo, A. A.The powdered leaf of Vernonia amygdalina was subjected to phytochemical screening, and in vitro antioxidant studies. The volatile oil of the leaves of the plant was also screened to determine the constituents. Analgesic tests using acetic acid induced writhing and paw licking (formalin) test in mice were also carried out. The in vitro antioxidant assay used include FRAP, ABTS, DPPH, and NO assay and then compared these with standards (Vitamin E and Rutin). Results showed the presence of saponins and tannins strongly, while alkaloids, flavonoids, anthraquinones and terpenoids were present in little quantities. On the other hand however, cardiac glycosides were absent in the plant. In the FRAP assay method, the absorbance of Vernonia amygdalina was found to be dose dependent with the maximum absorbance of 0.641nm at 0.5mg/ml which was significantly higher than that of rutin (0.56nm) and lower than that of Vitamin E (0.77nm). The ABTS radical scavenging activity of Vernonia amygdalina showed a dose dependent increase in the inhibition of the ABTS radical scavenging activity (91.93, 95.42, 99.24, 99.34 and 99.53% at 0.025, 0.05, 0.1, 0.2 and 0.5mg/ml respectively). This was comparable to that of rutin. The extract and the reference antioxidant (Rutin and Vitamin E) promoted an inhibition of DPPH radical at all concentrations tested in this study. Vernonia amygdalina showed a relatively stable effect in inhibiting the DPPH radical at all doses tested reaching 74.76%, 69.11% and 86.90% for Vernonia amygdalina, Vitamin E and Rutin respectively at the highest concentration. Vernonia amygdalina showed a dose dependent increase in the inhibition of the nitric oxide radical. The major compounds obtained from the GC-MS analysis of the essential of Vernonia amygdalina in this study were caryophyllene oxide (23.48%), phytol (22.92%), 2-Pentadecanone, 6,10,14-trimethyl (12.98%), hexadecanoic acid ethyl ester (12.24%), Oxirane, heptadecyl (12.11%), benzaldehyde (4.97%), benzeneacetaldehyde (5.83%), and trans-beta-ionone (5.47%). The methanol leaf extract of Vernonia amygdalina inhibited the acetic acid induced writhing in a manner comparable with the standard drug used in this study. The paw licking (formalin) test produces a distinct biphasic response to pain stimulus and the extract caused a dose dependent decrease in the inhibition of pain in both phases of the formalin paw lick test.Item Phytochemical, acute toxicity, analgesic, in vitro antioxidant studies and GC-MS investigation of essential oil of the methanol leaf extract of Momordica charantia(Sciencedomain International, 2017) Ofuegbe, S. O.; Akinrinde, A. S.; Oyagbemi, A. A.; Omobowale, T. O.; Yakubu, M. A.; Adedapo, A. A.Medicinal plants have bioactive compounds which play an important role in the healing of various diseases. They are the best sources for chemical ingredients, antimicrobial and antioxidant agents for cure of different diseases. Most medicinal plants possess pharmacological activities (anti-inflammatory, antidiabetic, antioxidant, antibacterial, antifungal etc.) due to the presence of these phytochemicals in them. In this study, we intend to conduct qualitative phytochemical screening and to quantitatively evaluate the total phenol, flavonols, tannins, proanthocyanidins and flavonoids contents of the plant, Mormodica charantia. The acute toxicity studies of the methanol leaf extract of M. charantia on mice was conducted to evaluate how safe the plant is in relation to dosage, and this is intended to establish the safety of the plant in mice with reference to OECD guidelines. Furthermore, the analgesic activity of the methanol leaf extract of M. charantia and the free radical scavenging activities of the plant in vitro were demonstrated using various standard procedures. We also intend to profile the major compounds present in the essential oil of the plant understudied using Gas Chromatography-Mass Spectrometry Analysis. Summarily, this study was aimed to investigate the phytochemical screening, acute toxicity, analgesic, in vitro antioxidant, as well as the chemical constituents in the essential oil of the methanol leaf extract of M. charantia.Item Cobalt Chloride-induced Hepatic and Intestinal damage in rats: Protection by ethyl acetate and chloroform fractions of Ocimum gratissimum2016(Informatics Publishing Limited, 2016) Akinrinde, A. S.; Oyagbemi, A. A.; Omobowale, T. O.; Nwozuzu, V. C.Cobalt chloride is known to produce symptoms of diarrhea, vomiting and other gastrointestinal disturbances. We investigated the potential roles of the ethyl acetate and chloroform fractions of Ocimum gratissimum (OG), traditionally used to treat diarrhea and other gastrointestinal disorders in protection against cobalt chloride (CoCl2)-induced liver and intestinal damage. Wistar albino rats were given CoCl2 (350 ppm) in drinking water for 7 days, alone or concurrently with either fractions of OG at 100 and 200mg/kg each. Gallic acid (120 mg/kg) was administered to a group of rats as a standard flavonoid. Biochemical indices of oxidative stress, antioxidant enzyme activities, the levels of pro-inflammatory cytokines (Interleukin 1β; IL-1β and Tumor necrosis factor, TNF-α) were evaluated and the histological appearance of the liver and intestinal mucosa was investigated. CoCl2 produced significant elevations (p<0.05) in hydrogen peroxide (H2O2), malondialdehyde (MDA), IL-1β, alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase (ALP). This was accompanied with significant reductions (p<0.05) in reduced glutathione (GSH), glutathione peroxidase (GPX) and glutathione S-transferase (GST) activities. Liver sections of rats exposed to CoCl2had poor architecture and areas of necrosis with several dead hepatocytes, while some appeared with hyperchromic nuclei. Intestinal mucosa showed significant loss of absorptive epithelial cells with CoCl2 exposure. Treatment with the fractions from OG produced reduction in H2O2, MDA and IL-1β levels; reduced serum activities of ALT, AST and ALP; restoration of GSH levels and improved activities of GPX and GST. The fractions significantly preserved the hepatic and intestinal architecture.Our results indicate that the fractions of OG exhibited considerable hepatic and intestinal protection by reduction in levels of oxidants and pro-inflammatory cytokines, enhancement of antioxidant enzyme activities and preservation of tissue integrity and might thus be very useful agents in protecting the liver and intestines during concurrent exposure to Cobalt chloride.Item Alterations in blood pressure, antioxidant status and caspase 8 expression in cobalt chloride-induced cardio-renal dysfunction are reversed by Ocimum gratissimum and gallic acid in Wistar rats(Elsevier GmbH, 2016) Akinrinde, A. S.; Oyagbemi, A. A.; Omobowale, T. O.; Asenuga, E. R.; Ajibade, T. O.The protective abilities of the chloroform extract of Ocimum gratissimum (COG) and gallic acid against cobalt chloride (CoCl2) − induced cardiac and renal toxicity were evaluated. Rats were exposed to CoCl2 (350 ppm) for 7 days, either alone, or in combination with COG (100 and 200 mg/kg) or gallic acid (120 mg/kg). CoCl2 given alone, caused significant increases (p < 0.05) in oxidative stress parameters (hydrogen peroxide, H2O2 and malondialdehyde, MDA) and increased expression of the apoptotic initiator caspase 8 in the heart and kidneys. There was significant reduction (p < 0.05) in reduced glutathione (GSH) in cardiac and renal tissues; reduction in superoxide dismutase (SOD) activity in the kidneys and adaptive increases in Glutathione S-transferase (GST) and catalase (CAT). CoCl2 also produced significant reduction (p < 0.05) in systolic (SBP), diastolic (DBP) and mean arterial (MAP) blood pressures. Oral COG and gallic acid treatment significantly reduced (p < 0.05) the levels of H2O2 and MDA; with reduced expression of caspase 8 and restoration of GSH levels, GPx, SOD and CAT activities, howbeit, to varying degrees in the heart and kidneys. COG (200 mg/kg) was most effective in restoring the blood pressures in the rats to near control levels. CoCl2-induced histopathological lesions including myocardial infarction and inflammation and renaltubular necrosis and inflammation were effectively ameliorated by the treatments administered. This study provides evidence for the protective roles of O. gratissimum and gallic acid by modulation of CoCl2-induced alterations in blood pressure, antioxidant status and pro-apoptotic caspase 8 in Wistar rats.Item Gallic acid ameliorates Cyclophosphamide-Induced neurotoxicity in Wistar rats through free radical scavenging activity and improvement in antioxidant defense system(Taylor & Francis Group, LLC, 2016) Oyagbemi, A. A.; Omobowale, T. O.; Saba, A. B.; Olowu, E. R.; Dada, R. O.; Akinrinde, A. S.Cyclophosphamide (CPA) is a widely used anticancer chemotherapeutic agent and its toxicity has been associated with its toxic metabolites phosphormide mustard. Therefore, the ameliorative effect of Gallic acid against neurotoxicity was examined in this study. Sixty rats were grouped into 10 rats per group. Group 1 received saline orally. Group 2 received CPA at 100 mg/kg single dose intraperitoneally on day 1. Groups 3 and 4 were treated with Gallic acid (GA) at 60 and 120 mg/kg body weight only for 10 days and also received a single dose of CPA (100 mg/kg) intraperitoneally on day 1, respectively. Rats in groups 5 and 6 received GA at 60 and 120 mg/kg body weight only for 10 days. Groups 3, 4, 5, and 6 received GA orally. The cerebellar and cerebral malondialdehyde (MDA) contents and hydrogen peroxide generation were significantly (p < .05) elevated. The cerebellar and cerebral catalase (CAT), superoxide dismutase and glutathione-S-transferase (GST) activities were significantly (p < .05) reduced in CPA treated group. The activity of glutathione peroxidase (GPx) was significantly increased in rats that were treatment with CPA. Also, nitrite content was significantly elevated in the brain of rats that received the toxic dose of CPA. All these findings suggest that treatment with GA (60 and 120 mg/kg) ameliorated the neurotoxicity induced by CPA via reduction of oxidative stress and increase in antioxidant defense system. Combining all, chemotherapeutic agents with structure/function similar to GA could be of potential benefit to the pharmaceutical industries as an adjuvant in chemotherapy with little or no side effects.Item Antioxidant potential of the methanol extract of Parquetina nigrescens mediates protection against intestinal Ischemia-Reperfusion injury in rats(Taylor & Francis Group, LLC, 2015) Akinrinmade, F. J.; Akinrinde, A. S.; Soyemi, O. O.; Oyagbemi, A. A.Parquetina nigrescens is a medicinal herb with recognized antioxidant properties and potential to alleviate conditions associated with oxidative stress, including gastric ulcers. We investigated the protective potential of methanol extract of Parquetina nigrescens (MEPN) against ischemia-reperfusion injury in the intestine of rats. Thirty (30) male Wistar albino rats were randomly assigned into five groups with Group I made up of control rats and Group II consisting of rats experimentally subjected to ischemia and reperfusion (IR) by clamping of the superior mesenteric artery (SMA) for 30 minutes and 45 minutes, respectively. Groups III and IV rats also had IR, but were initially pre-treated with MEPN at 500 mg/kg and 1000 mg/kg respectively, for seven days. Rats in Group V were also pre-treated with Vitamin C, for seven days, before induction of IR. The results showed marked reduction in intestinal epithelial lesions in groups treated with MEPN, compared to the IR group which had severe villi erosion, inflammatory cell infiltration and hemorrhages. There were significant increases in Malondialdehyde (MDA) and significant reductions in reduced glutathione (GSH) and Glutathione S-transferase (GST) activity with IR injury, while pre-treatment with either MEPN or Vitamin C prevented these effects. Increases in Glutathione peroxidase (GPX), Catalase (CAT) and Superoxide dismutase (SOD) with IR provided evidence for adaptive responses to oxidative injury during IR and preservation of enzyme activity by MEPN and Vitamin C. Taken together, Parquetina nigrescens provided considerable alleviation of intestinal injury produced by IR, at values much as effective as that offered by Vitamin C.Item Changes in serum cytokine levels, hepatic and intestinal morphology in aflatoxin B1-induced injury: modulatory roles of melatonin and flavonoid-rich fractions from Chromolena odorata(Springer, 2015) Akinrinmade, F. J.; Akinrinde, A. S.; Amid, A.Aflatoxins are known to produce chronic carcinogenic, mutagenic, and teratogenic effects, as well as acute inflammatory effects, especially in the gastrointestinal tract. The potentials of the flavonoid-rich extract from Chromolena odorata (FCO) and melatonin (a standard anti-oxidant and anti-inflammatory agent) against aflatoxin B1 (AFB1)-induced alterations in pro-inflammatory cytokine levels and morphology of liver and small intestines were evaluated in this study. We utilized Wistar albino rats (200–230 g) randomly divided into five groups made up of group A, control rats; group B, rats given AFB1 (2.5 mg/kg, intraperitone al) twice on days 5 and 7; rats in groups C, D, and E were treated with melatonin (10 mg/kg, intraperitoneal) or oral doses of FCO1 (50 mg/kg) and FCO2 (100 mg/kg) for 7 days, respectively, along with AFB1 injection on days 5 and 7. Serum levels of interleukin 1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α) were determined using commercial ELISA kits and histopathological evaluation of the liver, duodenum, and ileum were also carried out. We observed significant elevation (p < 0.05) in serum IL-1β correlating with hemorrhages and leucocytic and lymphocytic infiltration in the liver and intestines as evidences of an acute inflammatory response to AFB1 administration. All treatments yielded significant reduction (p < 0.05) in IL-1β levels, although TNF-α levels were not significantly altered in all rats that received AFB1, irrespective of the treatments. Melatonin and FCO2 produced considerable protection of hepatic tissues, although melatonin was not quite effective in protecting the intestinal lesions. Our findings suggest a modulation of cytokine expression that may, in part, be responsible for the abilities of C. odorata or melatonin in amelioration of hepatic and intestinal lesions associated with aflatoxin B1 injury.
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