Scholarly works in Veterinary Surgery and Reproduction
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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 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.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 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.Item Nephroprotective effect of methanol extract of Moringa oleifera leaves on acute kidney injury induced by ischemia-reperfusion in rats(Faculty of Medicine, Makerere University., 2020) Akinrinde, A. S.; Oduwole, O.; Akinrinmade, F. J.; Bolaji-Alab, F. B.Background: Moringa oleifera is known to exhibit protection against oxidative damage due to its rich content of compounds with antioxidant activity. This study investigated the protective effect of the methanol extract of Moringa oleifera (MO) in a rat model of renal ischemia-reperfusion (IR) injury. Methods: Forty two wistar rats were randomly assigned to six groups of seven rats each, as follows: A, control group; B, sham-operated group; C, IR group; D, IR + low dose (200 mg/kg) MO; E, IR + high dose (400 mg/kg) MO and F, IR + Vitamin C (200 mg/kg). Unilateral ischaemia was induced by occluding the left renal artery for 45 minutes followed by rep erfusion up to 24 hours. Results: Moringa oleifera significantly (p<0.05) ameliorated IR-induced increases in malondialdehyde (MDA), protein carbon yls (PC) and advanced oxidation protein products (AOPP), while also decreasing serum BUN and Creatinine levels. Moreover, the low dose of MO caused reductions in renal NO and H2O2 levels, while increasing renal GPx and GST activities. Histopathology revealed marked improvement of tissue alterations induced by IR with both doses of MO. Conclusion: Overall, the methanol extract of M. oleifera effectively attenuated the deleterious effects of renal IR via alleviation of tissue oxidative stress.Item Acute aflatoxin B1-induced gastro-duodenal and hepatic oxidative damage is preceded by time-dependent hyperlactatemia in rats(Springer, 2020) Akinrinde, A. S.; Ogunbunmi, T.; Akinrinmade, F. J.Elevated serum lactate concentration has been used to predict the risk of fatality in various disease states in acutely ill patients or poisoning with different chemicals. However, its utility in predicting disease progression during acute aflatoxicosis has not been investigated. This study was designed to evaluate changes in blood lactate levels following acute exposure to aflatoxin B1 (AFB1) and to determine whether changes in blood lactate levels bear any relationship with biochemical and/or morphological lesions in the stomach, duodenum, and liver. Twenty-one male Wistar rats were randomly divided into three groups (n = 7 rats /group) including Group A (control) receiving vehicle alone and Groups B and C treated with single oral doses of AFB1 at 2.5 and 5 mg/kg, respectively. AFB1 produced significant (p < 0.05) time- and dose-dependent increase in blood lactate concentration as early as 1 h following its administration, with further increases observed at 3 h and 6 h. The hyperlactatemia accompanied tissue oxidative changes including increased H2O2 and MDA, as well as depletion in glutathione, glutathione peroxidase, superoxide dismutase, and total thiols in gastro-duodenal and hepatic tissues. The oxidative changes were reflected in morphological alterations observed at histopathology with more severe lesions observed with the higher dose of AFB1. Serum levels of pro inflammatory cytokines (TNF-α and IL-1β) were, however, differently modified by AFB1 administration. Taken together, the results from this study gives indication that hyperlactatemia may find utility in predicting the severity of tissue damage induced by acute AFB1 exposure.Item Prevalence of rumen impaction with non-biodegrable materials in cattle in Ibadan, Nigeria(Nigerian Society for Animal Production, 2021) Akinrinmade, J. F; Akinrinde, S. A.A study was conducted on 3031 cattle slaughtered in Ibadan over a period of three months to determine the prevalence of rumen impaction with indigestible garbage and evaluate breed, sex, age and some blood indices as risk factors. Thorough antemortem and postmortem examinations were carried out on each of the animals to determine the breed, health status, sex, age and presence of indigestible garbage in the rumen while blood samples were collected and analysed only for animals with indigestible garbage, to determine total serum protein and phosphorus levels. Results showed overall prevalence of rumen impaction was 10.77% and it differed significantly between breeds, but was highest in the Red Bororo (RB). Sex and age had significant influence on the prevalence of rumen impaction. It was significantly higher (P < 0.05) in females than in males and in older animals than in younger ones. Total serum protein and phosphorus levels were significantly lower than reference values in animals with rumen impaction.Item Multiple Organ Dysfunction Syndrome: Phytotherapeutic evidences from intestinal ischemia-reperfusion models(Apple Academic Press, 2023) Akinrinde, A. S.; Akinrinmade, J. F.The gastrointestinal mucosa serves important barrier and defensive function against pathogenic bacteria, aggressive factors, and other inflammatory stimuli present within the lumen of the intestines. A variety of pathological and/or surgical conditions, known to produce intestinal ischemia-reperfusion injury (HRI) (e.g., hemorrhagic shock, strangulated bowel, intussusception, and volvulus) has been associated with breaches in gut barrier integrity, increased barrier permeability, and translocation of viable enteric bacteria and their toxins into the portal and systemic circulation. The result of this trans-epithelial movement of enteric microbes and/or toxins is the generalized activation of various inflammatory mediators (e.g., cytokines, reactive oxygen species, leucocytes, and the complement system) in what is often described as the systemic inflammatory response syndrome (SIRS). One devastating consequence of IIRI and SIRS is widespread injury to remote organs, a condition often referred to as multiple organ dysfunction syndrome (MODS), which is the leading cause of mortality in critically ill patients, especially those in intensive care units. From the foregoing, it has been suggested that compounds that combine multiple activities such as antibacterial, anti-inflammatory, antioxidant, and immune-modulatory roles, may provide new approaches to the prevention and/or treatment of MODS. In this regard, medicinal herbs with their composite nature of bioactivities due to several inherent phytochemicals are being investigated at different levels for their benefits in modulating the pathophysiological mechanisms that give rise to MODS. With particular reference to animal models of IIRL this chapter explores available experimental evidence of the potential prophylactic and/or therapeutic benefits of medicinal herbs in limiting remote organ dysfunction arising from gastrointestinal injury.