Browsing by Author "Adunmo G.O."

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    EFFECTS OF PHOSPHODIESTERASE 5 INHIBITOR (VIAGRA) ON BIOCHEMICAL PARAMETERS OF L NAME-INDUCED TESTICULAR TOXICITY IN ADULT MALE WISTAR RATS
    (KJHS, 2024) Adunmo G.O.; Oyewopo A.O.; Akindehin O.A.; Stephen D.A; Ogunbiyi O.E.; Abdulazeez I.A.; Lawal A.Z.; Adeleke O.S; Akingbade A.M.; Opoola F.O.; Ajayi S.O.; Ajayi A.J.
    ABSTRACT Testicular toxicity is a growing concern in today's world, with various factors contributing to its prevalence. Nitric oxide (NO) imbalance, often induced by N (gamma)-nitro-L-arginine methyl ester (L-NAME), is a significant factor associated with testicular dysfunction. Sildenafil (Viagra), a phosphodiesterase type 5 inhibitor, has shown promise in improving testicular function by modulating NO levels. This study aimed to investigate the role of Sildenafil (Viagra) on biochemical parameters of L-NAME induced testicular toxicity in Wistar rats. Twenty-four adult male Wistar rats were divided into four groups: Control (physiological saline-treated), L-Name (L-Name-induced testicular toxicity), PDE (Sildenafil-treated), and L-Name + Sildenafil (co-treatment) and subjected to a 56-day treatment regimen. At the end of the administration, the animals were sacrificed, tissues collected and biochemical and histological assessments were performed. Findings revealed that L-Name administration led to a significant decreased in nitric oxide levels, follicle stimulating hormone, luteinizing hormone, testosterone and increase in oxidative stress when compared to the control group. Furthermore, histological analysis demonstrated structural alterations in the testes of L NAME-treated rats, indicative of testicular toxicity. Rats treated with Sildenafil showed a slight reversal of these adverse effects. Also, slight reversals of impaired spermatogenesis were evident in the co-treatment group. This study provides compelling evidence for the potential therapeutic role of sildenafil in ameliorating L-NAME-induced testicular toxicity in adult male Wistar rats. Keywords: Testicular toxicity, spermatogenesis, oxidative stress, testosterone.
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    Moringa oleifera ameliorates cuprizone-induced cerebellar damage in adult female rats
    (Research Journal of Health Sciences, 2018) Omotoso G.O.; Kadir R.E.; Lewu S.F.; Gbadamosi I.T; Akinlolu A.A.; Adunmo G.O.; Kolo R.M.; Lawal M.O; Ameen M.O.
    Objectives: Cuprizone is a neurotoxicant used in modeling demyelinating disorders. This study explored the effects of Moringa oleifera (MO) on oxidative, histomorphological and behavioural changes in cuprizone-damaged cerebellum. Methods: Twenty adult female Wistar rats were grouped into 4, each group having five animals. Group A received 1 ml of normal saline (Control); group B received 0.4% cuprizone; group C received 15.6 mg/kgBW Moringa oleifera leaf extract; group D received 0.4% cuprizone and 15.6 mg/kgBW Moringa oleifera, orally for 5 weeks. The animals were assessed for exploratory and locomotor activities, while the cerebellum was processed for histology and assayed for nitric oxide (NO), catalase (CAT) and superoxide dismutase (SOD) activities. Results: Cuprizone treatment caused weight reduction, disruption of Purkinje cell layer, cellular degeneration, reduction in NO, CAT and SOD activities. However, these changes were ameliorated when co-administered with MO. Conclusion: The anti-oxidative property of Moringa oleifera is responsible for its ameliorative effect in cuprizone neurotoxicity. Keywords: demyelination, cuprizone, cerebellar damage, Moringa oleifera, oxidative enzymes
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    Moringa oleifera ameliorates cuprizone-induced cerebellar damage in adult female rats
    (College of Health Sciences, Osun State University, 2018) Omotoso G.O.; Kadir R.E.; Lewu S.F.; Gbadamosi I.T.; Akinlolu A.A.; Adunmo G.O.; Kolo R.M.; Lawal M.O.; Ameen M.O.
    Objectives: Cuprizone is a neurotoxicant used in modeling demyelinating disorders. This study explored the effects of Moringa oleifera (MO) on oxidative, histomorphological and behavioural changes in cuprizone-damaged cerebellum. Methods: Twenty adult female Wistar rats were grouped into 4, each group having five animals. Group A received 1 ml of normal saline (Control); group B received 0.4% cuprizone; group C received 15.6 mg/kgBW Moringa oleifera leaf extract; group D received 0.4% cuprizone and 15.6 mg/kgBW Moringa oleifera, orally for 5 weeks. The animals were assessed for exploratory and locomotor activities, while the cerebellum was processed for histology and assayed for nitric oxide (NO), catalase (CAT) and superoxide dismutase (SOD) activities. Results: Cuprizone treatment caused weight reduction, disruption of Purkinje cell layer, cellular degeneration, reduction in NO, CAT and SOD activities. However, these changes were ameliorated when co-administered with MO. Conclusion: The anti-oxidative property of Moringa oleifera is responsible for its ameliorative effect in cuprizone neurotoxicity.
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    Moringa oleifera attenuates biochemical and histological changes associated with the pancreas in nicotine-treated rats
    (Research Journal of Health Sciences, 2018) Omotoso G.O.; Adunmo G.O.; Ojulari L.S.; Olawuyi T.S.; Lewu F.S. ,; Jaji-Sulaimon R.; Sulaimon F.A.; Gbadamosi I.T. ,; Onoja O.P.
    Objective: The study was undertaken in order to evaluate the beneficial potential of Moringa oleifera, in nicotine-induced pancreatic injury. Method: Forty-five adult female albino rats were divided into 5 groups A-E, each group having nine rats. Group A received normal saline; group B received 6.88 mg/kg of nicotine intraperitoneally (i.p); group C received 6.88 mg/kg of nicotine i.p. and 200 mg/kg of Moringa oleifera leaf powder dissolved in 2 ml of normal saline (orally); group D received 13.76 mg/kg of nicotine i.p., while group E received 13.76 mg/kg of nicotine i.p. and 200 mg/kg of Moringa oleifera leaf powder dissolved in 2 ml of normal saline (orally). Treatment was for 8 days and the rats were sacrificed after 24 hours of termination of study. Intracardial blood specimens were obtained to analyse blood glucose, while the pancreas was excised and either fixed in 4% paraformaldehyde for histology or sucrose solution and homogenised for biochemical analysis of lactate dehydrogenase (LDH) and glucose-6-phosphate dehydrogenase (G-6-PDH) enzymes. Results: In comparison with the Control, animals treated with low dose of nicotine with or without Moringa oleifera and those treated with high dose of nicotine plus Moringa oleifera had reduction in body weights (p>0.05), while marked reduction in pancreatic weights was noted in low dose nicotine (p<0.05) and both nicotine groups co-treated with Moringa oleifera (p<0.05). There were no significant changes in the levels of blood glucose and pancreatic G-6-PDH levels, while significant reduction occurred in pancreatic LDH levels in nicotine-treated rats (p<0.05). However, LDH improved following co administration with Moringa oleifera. Observation of the histology of the pancreas revealed atrophy of intercalated ducts, poorly delineated and disintegrating islet of Langerhans in animals treated with the higher dose of nicotine, while changes in pancreatic tissue in animals co-treated with Moringa oleifera were not as severe as the nicotine-treated animals. Conclusion: Moringa oleifera leaf decoction minimally ameliorates morphological and biochemical changes associated with nicotine-induced pancreatic damage. Keywords: Nicotine, Pancreatic damage, Moringa oleifera