Scholarly works in Veterinary Surgery and Reproduction
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Item 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.Item Glycine and L-Arginine supplementation ameliorates gastro-duodenal toxicity in a rat model of NSAID (Diclofenac)-gastroenteropathy via inhibition of oxidative stress(Walter de Gruyter GmbH, 2021) Akinrinde, A. S.; Hameed, H. O.Objectives: This study examined the possible protective roles of exogenous glycine (Gly) and L-Arginine (L-Arg) against Diclofenac (DIC)-induced gastro-duodenal damage in rats. Methods: Rats were divided into Group A (control), Group B (DIC group) and Groups C–F which were pre-treated for five days with Gly1 (250 mg/kg), Gly2 (500 mg/kg), L-Arg1 (200 mg/kg) and L-Arg2 (400 mg/kg), respectively, before co-treatment with DIC for another three days. Hematologi cal, biochemical and histopathological analyses were then carried out. Results: DIC produced significant (p<0.05) reduction in PCV (13.82%), Hb (46.58%), RBC (30.53%), serum total protein (32.72%), albumin (28.44%) and globulin (38.01%) along with significant (p<0.05) elevation of serum MPO activity (83.30%), when compared with control. In addition, DIC increased gastric H2O2 and MDA levels by 33.93 and 48.59%, respectively, while the duodenal levels of the same parameters increased by 19.43 and 85.56%, respectively. Moreover, SOD, GPx and GST activities in the DIC group were significantly (p<0.05) reduced in the stomach (21.12, 24.35 and 51.28%, respectively) and duodenum (30.59, 16.35 and 37.90%, respectively), compared to control. Treatment with Gly and L-Arg resulted in significant amelioration of the DIC-induced alterations although L-Arg produced better amelioration of RBC (29.78%), total protein (10.12%), albumin (9.93%) and MPO (65.01%), compared to the DIC group. The protective effects of both amino acids against oxidative stress parameters and histological lesions were largely similar. Conclusions: The data from this study suggest that Gly or L-Arg prevented DIC-induced gastro-duodenal toxicity and might, therefore be useful in improving the therapeutic index of DIC.Item Glycine and L-Arginine supplementation ameliorates gastro-duodenal toxicity in a rat model of NSAID (Diclofenac)-gastroenteropathy via inhibition of oxidative stress(Walter de Gruyter GmbH, 2021) Akinrinde, A. S.; Hameed, H. O.Objectives: This study examined the possible protective roles of exogenous glycine (Gly) and L-Arginine (L-Arg) against Diclofenac (DIC)-induced gastro-duodenal damage in rats. Methods: Rats were divided into Group A (control), Group B (DIC group) and Groups C–F which were pre-treated for five days with Gly1 (250 mg/kg), Gly2 (500 mg/kg), L-Arg1 (200 mg/kg) and L-Arg2 (400 mg/kg), respectively, before co-treatment with DIC for another three days. Hematologi cal, biochemical and histopathological analyses were then carried out. Results: DIC produced significant (p<0.05) reduction in PCV (13.82%), Hb (46.58%), RBC (30.53%), serum total protein (32.72%), albumin (28.44%) and globulin (38.01%) along with significant (p<0.05) elevation of serum MPO activity (83.30%), when compared with control. In addition, DIC increased gastric H2O2 and MDA levels by 33.93 and 48.59%, respectively, while the duodenal levels of the same parameters increased by 19.43 and 85.56%, respectively. Moreover, SOD, GPx and GST activities in the DIC group were significantly (p<0.05) reduced in the stomach (21.12, 24.35 and 51.28%, respectively) and duodenum (30.59, 16.35 and 37.90%, respectively), compared to control. Treatment with Gly and L-Arg resulted in significant amelioration of the DIC-induced alterations although L-Arg produced better amelioration of RBC (29.78%), total protein (10.12%), albumin (9.93%) and MPO (65.01%), compared to the DIC group. The protective effects of both amino acids against oxidative stress parameters and histological lesions were largely similar. Conclusions: The data from this study suggest that Gly or L-Arg prevented DIC-induced gastro-duodenal toxicity and might, therefore be useful in improving the therapeutic index of DIC.Item Exacerbation of diclofenac-induced gastroenterohepatic damage by concomitant exposure to sodium fluoride in rats: protective role of luteolin(Informa UK Limited, 2020) Akinrinde, A. S.; Soetan, K. O.; Tijani, M. O.NSAID-induced gastrointestinal toxicity is associated with non-selective inhibition of cyclooxygenase (COX)-mediated synthesis of prostaglandins. Fluoride salts, known to stimulate COX-2 synthesis, have also been associated with gastrointestinal damage. The effects of fluoride treatment on NSAID toxicity are, however, yet to be clarified. This study examined the effect of sodium fluoride (NaF) on diclofenac (DIC)-induced gastroduodenal and hepatic toxicity in rats. In addition, the potential protective role of Luteolin (Lut), an antioxidant and anti-inflammatory flavonoid, in co-exposure to NaF and DIC was also investigated. Five groups of rats were treated thus: Group A (control): distilled water vehicle for 8 days; Group B: DIC (9 mg/kg) orally, twice daily from days 6 to 8; Group C: NaF (300 ppm) plus DIC for the final 3 days; Groups D and E: Luteolin at 100 mg/kg and 200 mg/kg, respectively, with concurrent NaF and DIC exposures. Rats co-treated with DIC and NaF exhibited the highest severity of dark watery diarrhea and gastroduodenal hemorrhages. NaF aggravated the DIC-induced increases in malondialde hyde (MDA), advanced oxidation protein products (AOPP), protein carbonyls (PC), H2O2, and nitric oxide, while inhibiting glutathione peroxidase (GPx) and glutathione S-transferase (GST) in all the tis sues. In contrast, Luteolin treatment significantly attenuated the gastroduodenal and hepatic damage caused by NaF and DIC co-administration by suppressing oxidative damage and lesions in the tissues. These results show, for the first time, that NaF may enhance diclofenac-induced gastrointestinal toxicity and also suggest that Luteolin may be a promising lead for the treatment of drug-induced gastroenteropathy.Item Exacerbation of diclofenac-induced gastroenterohepatic damage by concomitant exposure to sodium fluoride in rats: protective role of luteolin(0148-0545, 2020) Akinrinde, A. S.; Soetan, K. O.; Tijani, M. O.NSAID-induced gastrointestinal toxicity is associated with non-selective inhibition of cyclooxygenase (COX)-mediated synthesis of prostaglandins. Fluoride salts, known to stimulate COX-2 synthesis, have also been associated with gastrointestinal damage. The effects of fluoride treatment on NSAID toxicity are, however, yet to be clarified. This study examined the effect of sodium fluoride (NaF) on diclofenac (DIC)-induced gastroduodenal and hepatic toxicity in rats. In addition, the potential protective role of Luteolin (Lut), an antioxidant and anti-inflammatory flavonoid, in co-exposure to NaF and DIC was also investigated. Five groups of rats were treated thus: Group A (control): distilled water vehicle for 8 days; Group B: DIC (9 mg/kg) orally, twice daily from days 6 to 8; Group C: NaF (300 ppm) plus DIC for the final 3 days; Groups D and E: Luteolin at 100 mg/kg and 200 mg/kg, respectively, with concurrent NaF and DIC exposures. Rats co-treated with DIC and NaF exhibited the highest severity of dark watery diarrhea and gastroduodenal hemorrhages. NaF aggravated the DIC-induced increases in malondialde hyde (MDA), advanced oxidation protein products (AOPP), protein carbonyls (PC), H2O2, and nitric oxide, while inhibiting glutathione peroxidase (GPx) and glutathione S-transferase (GST) in all the tis sues. In contrast, Luteolin treatment significantly attenuated the gastroduodenal and hepatic damage caused by NaF and DIC co-administration by suppressing oxidative damage and lesions in the tissues. These results show, for the first time, that NaF may enhance diclofenac-induced gastrointestinal toxicity and also suggest that Luteolin may be a promising lead for the treatment of drug-induced gastroenteropathy.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 Effect of exposure and withdrawal on Lead-induced toxicity and oxidative stress in cardiac tissues of Rats(Informatics Publishing Limited, 2016) Omobowale, T. O.; Oyagbemi, A. A.; Akinrinde, S. A.; Ola-Davies, O. E.; Saba, A. B.; Olopade, J. O.; Adedapo, A. A.Lead poisoning continues to pose a serious health challenge and more significantly so in developing countries with ineffective waste disposal systems. Recent efforts at solving lead poisoning issues have seen entire towns being resettled from lead-contaminated areas. This study was designed to investigate whether withdrawal of lead exposure results in a resolution of toxic effects of lead in cardiac tissues. Adult male Wistar rats were exposed orally to lead acetate (PbA) at doses of 0.25, 0.5, and 1.0 mg/ml for 6-week duration, after which one-half was sacrificed and the remaining left for a further 6 weeks without lead treatment. Exposure of rats to PbA produced significant decline (P < 0.05) in the activities of antioxidant parameters, including superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione-S-transferase (GST), catalase (CAT), and reduced glutathione (GSH), whereas malondialdehyde (MDA) concentration was significantly elevated. Animals from the withdrawal period exhibited a similar pattern of alterations, with a significant (P < 0.05) reduction in GSH, GPx, and SOD and a significant elevation in MDA and H2 O2 concentrations. However, GST activity was elevated, whereas CAT activity remained unaltered in the withdrawal period. The results of this study showed that cardiotoxicity indicated by induction of oxidative stress and reduction in antioxidant parameters failed to resolve upon withdrawal of lead exposure in male rats during the period of study.Item Protective effects of kolaviron and gallic acid against cobalt-chloride-induced cardiorenal dysfunction via suppression of oxidative stress and activation of the ERK signaling pathway(Canadian Science Publishing, 2016) Akinrinde, S. A.; Omobowale, O.; Oyagbemi, A.; Asenuga, E.; Ajibade, T.Cobalt (Co) toxicity is a potential public health problem due to recent renewed use of Co in orthopedic implants, dietary supplements, and blood doping in athletes and horses. We investigated the protective roles of kolaviron (KV), a bi flavonoid of Garcinia kola, and gallic acid (GA) on cobalt chloride (CoCl2)-induced cardiorenal damage in rats. CoCl2 caused significant increases (p < 0.05) in serum creatine kinase–myocardial band (CK-MB), lactate dehydrogenase (LDH), aspartate transaminase (AST), xanthine oxidase (XO), urea, creatinine, malondialdehyde, H2O2, nitric oxide, as well as C-reactive protein expression, along with significant (p < 0.05) reduction in cardiac and renal expression of extracellular signal regulated kinase (ERK) and the activities of superoxide dismutase, catalase, and glutathione S-transferase. KV and GA prevented the toxic effects of CoCl2 by stimulating ERK expression and reversing Co-induced biochemical changes. Administration of CoCl2 alone did not significantly alter ECG patterns in the rats, although co-treatment with KV (200 mg/kg) produced QT-segment prolongation and also appeared to potentiate Co hypotension. Histopathology of the heart and kidneys of rats treated with KV and GA confirmed the biochemical data. KV and GA thus protected against cardiac and renal damage in Co intoxication via antioxidant and (or) cell survival mechanisms, possibly involving ERK activation.Item Cyclophosphamide‑induced hepatotoxicity in Wistar rats: The modulatory role of Gallic Acid as a hepatoprotective and chemopreventive phytochemical(Wolters Kluwer - Medknow, 2016) Oyagbemi, A. A.; Omobowale, O. T.; Asenuga, E. R.; Akinleye, A. S.; Ogunsanwo, R. O.; Saba, A. B.Background: Gallic acid (GA) is an endogenous plant phenol known to have antioxidant, free radical scavenging ability, anti inflammatory, anti cancer, and anti fungal properties. The aim of this study was to assess the protective effect of GA on cyclophosphamide (CPA) induced hepatotoxicity in male Wistar rats. Methods: Sixty rats were grouped into six groups of 10 rats per group. Group 1 received distilled water. Group 2 received CPA at 200 mg/kg single dose intraperitoneally on day 1. Groups 3 and 4 received a single dose of CPA (200 mg/kg) intraperitoneally on day 1 and then were treated with GA at 60 and 120 mg/kg body weight for 14 days, respectively. Rats in Groups 5 and 6 only received GA at 60 and 120 mg/kg body weight for 14 days, respectively. GA was administered orally. Results: CPA induced hepatic damage as indicated by significant elevation (P < 0.05) in aspartate aminotransferase, organ weight, and evidence by the histological study. CPA also induced hepatic oxidative stress as indicated by significant elevation (P < 0.05) in malondialdehyde content, hydrogen peroxide (H2 O2 ) generation, nitrite level, and the level of glutathione (GSH) peroxidase crashed in the CPA treated group. GA enhanced the antioxidant defense system as indicated by significant elevation (P < 0.05) in GSH level, catalase activity, and GSH S transferase activity. Conclusions: Taken together, the result of this present study shows that GA has a protective effect on CPA induced hepatotoxicity.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.