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  1. Home
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Browsing by Author "Asuku, A.O."

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  • Item
    Ameliorative Effect of Vitamin C and N-Acetyl cysteine on Mercury chloride-induced Neurotoxicity in Male Wistar Rats
    (Ibadan Biomedical Communication Group., 2024) Asuku, A.O.; Ayinla M.T; Ajibare, A.O.; Saliu, S.B.; Ogungbangbe, G.O.; Abejide M.; Awoyale O.
    The present study investigated the ameliorative effects of Vitamin C (Vit. C) and N-acetylcysteine (NAC) on mercury chloride (HgCl2)-induced neurotoxicity in male Wistar rats. Twenty (20) male Wistar rats were randomly grouped into four, n=5. I: control, received 0.5mL normal saline, II: received HgCl2 alone (5mg/kg), III: received HgCl2 (5mg/kg) plus Vit. C (100 mg/kg), IV: received HgCl2 (5mg/kg) and N-acetylcysteine (NAC) (50mg/kg) for fourteen (14) days. All the drugs were administered orally. The rats were subjected to behavioural tests (Morris water maze, novel object recognition, light and dark box, fore limb grip strength and beam walking balance tests). The rats were then euthanized to obtain brain tissues for the determination of catalase activity, total protein and nitric oxide (NO) levels. The result revealed a significant (P<0.05) increase in the escape latency, beam walking latency, and footslip scores, and a significant (P<0.05) decrease in the recognition ratio, exploration frequency, and drop-off time in the rats that were exposed to HgCl2 only. However, Vit. C and NAC reversed the observed behavioural deficits. Similarly, HgCl2 exposure caused a significant (P<0.05) decrease in the brain catalase and total protein, and a significant (P<0.05) increase in the NO level. Also, administration of Vit. C and NAC significantly (P<0.05) reversed the trend. This study concludes that Vit. C and NAC ameliorated HgCl2-induced neurotoxicity via attenuation of behavioural deficits and oxidative stress
  • Item
    Androgenic Effects of Aqueous seed extract of Moringa oleifera in Male Wistar Rats
    (Published by School of Medicine and Health Sciences, University of Papua, New Guinea, 2022) Ayinla M.T; Muhammad, A.S.; Ayinde, T.O.; Ojulari, L.S.; Owoyele, B.V.; Asuku, A.O.; Adebisi, R.O.; Badmus, O.A.; Krishnamurthy, R.
    Androgenic effects of Aqueous Seed-extract of Moringa oleifera (ASMO) in male Wistar rats were investigated. Eighteen (18) male Wistar rats weighing 200-240g were used for this study. The rats were divided into three (3) groups: Control (Group 1) that received 10 ml/kg of normal saline, Group 2: received low dose of ASMO (200mg/kg), and Group 3: received high dose of ASMO (500mg/kg). The animals were treated for twenty-eight days. On the 29th day, the rats were sacrificed and the testes were carefully removed for semen and biochemical analysis. Body weight, reproductive and vital organ weights were determined. Sperm parameters (motility, morphology, count and viability), tissue testosterone, luteinizing hormone (LH), Malondialdehyde (MDA) and Catalase were also determined using standard methods. Data were analysed using one-way ANOVA followed by Duncan new multiple range post hoc test. The result showed ASMO significantly increased (p<0.05) the final body weight, weight of reproductive and vital organs. Moreover, 200mg/kg body weight dose of ASMO significantly increased (p<0.05) the sperm parameters but 500mg/kg body weight dose significantly decreased it. ASMO also caused a significant dose dependent increase (p<0.05) in testosterone and catalase level but a significant decrease (p<0.05) in MDA and LH level compared with the control. In conclusion, this study revealed that ASMO has androgenic effects in male rats and thus provides a basis for the traditional use of Moringa oleifera in the management of male sexual disorders.
  • Item
    Aqueous Leaf Extract of Cola Acuminata (Malvaceae) Modulates Cholinergic Neurotransmission in Scopolamine-induced Memory Impairment in Male Wistar Rats.
    (The Society for Experimental Biology of Nigeria,, 2022) Ayinla M.T; Asuku, A.O.; Bangwai, T. B.; Owoyele, B.V.
    This study investigated the effects of aqueous leaf extract of Cola acuminata (ALECA) on cholinergic neurotransmission in scopolamine-induced rat model of memory impairment. A total of thirty-five male Wistar rats (178 12.32 g) were allotted into 7 groups (I–VII) at random as follows: I: control, received 5ml/kg body weight (body wt) of distilled water, II: received scopolamine alone (3mg/kg body wt), III: received Donepezil (2mg/kg body wt) plus scopolamine (3mg/kg body wt), IV: received Cola acuminata (50mg/kg body wt) plus scopolamine (3mg/kg body wt), V: received Cola acuminata, (100mg/kg body wt) plus scopolamine (3mg/kg body wt), VI: received Cola acuminata (300mg/kg body wt) plus scopolamine (3mg/kg body wt), VII: received Cola acuminata (400mg/kg body wt) plus scopolamine (3mg/kg body wt) for seven days. ALECA and distilled water were orally administered daily while scopolamine was injected intraperitoneally daily for seven days. Behavioural test were conducted using Morris water maze, light and dark box to assess learning and memory. Acetylcholinesterase (AchE) activity in the brain was assayed using Ellman’s method. Scopolamine caused a significant impairment in memory through decreased probing frequency and increase in escape latency time (memory index) in Light and Dark Box and Morris Water Maze respectively. Treatment with different doses of ALECA prevented cognitive impairment induced by scopolamine through increased probing frequency and decrease in escape latency time. However, this effect is not dose dependent and it compares favourably with the donepezil group (reference drug) The mechanism of action of ALECA was also investigated through estimation of brain Acetylcholine esterase. We found that the brain’s acetylcholinesterase activity significantly increased in response to scopolamine. While a significant (p<0.05) decline in acetylcholinesterase activity was seen after treatment with ALECA., and this effect compares favourably with donepezil group. The effect of ALECA is also not dose dependent. This study concludes that ALECA treatment could improve memory function in scopolamine-induced model of dementia through the inhibition of acetylcholine esterase activity.
  • Item
    Cola acuminata mitigates cognitive deficit and oxidative stress in mercury chloride-induced neurotoxicity in male Wistar rats
    (The Neuroscience Society of Nigeria., 2023) Asuku, A.O.; Ayinla M.T; Olajide, T. S.; Yakub, Z.; Owoyele, B.V.
    Cola acuminata is used in traditional medicine for the management of memory impairment and other neurodegenerative conditions. This study investigated the effects of Cola acuminata aqueous leaves extract (ALECA) on mercury chloride-induced neurotoxicity in Wistar rats. Twenty male Wistar rats weighing between 160 and 210 g were randomly assigned to four groups (n = 5). The control group received 0.5 mL of distilled water; the mercury chloride (HgCl2) group received HgCl2 (5 mg/kg b.w.); the ALECA100 and ALECA300 groups received ALECA (100 and 300 mg/kg b.w., respectively), followed by the administration of HgCl2 (5 mg/kg b.w.) for two weeks. The rats were subjected to behavioural tests in the Morris water maze and light and dark field box. The rats were then sacrificed to obtain their brains, which were homogenized for biochemical assays of acetylcholinesterase (AChE), malondialdehyde (MDA), total protein (TP), and glutathione (GSH) using standard methods. The results revealed a significant increase in escape latency, a significant decrease in probing frequency and brain GSH, and a significant (p<0.05) increase in brain MDA and TP levels and AChE activity in the rats exposed to HgCl2. However, administration of either 100 or 300 mg/kg ALECA protected against memory impairment with a significantly reduced escape latency, increased probing frequency and brain GSH, and decreased (p<0.05) MDA, TP and AChE. This study concludes that ALECA mitigated HgCl2- induced neurotoxicity via reduction of oxidative stress and enhanced cholinergic functions.
  • Item
    Melatonin and Vitamin C modulate cholinergic neurotransmission and oxidative stress in scopolamine-induced rat model of dementia
    (African Association of Physiological Sciences, 2020) Ayinla M.T; Asuku, A.O.; Bayo-olugbami, A.; Ayeni, O.A.; Abiola, A.A.; Owoyele, B.V.
    Background: Cognitive dysfunction which characterizes dementia is reportedly caused by multiple factors including oxidant-antioxidant imbalance, inflammation, alteration in synaptic neurotransmission. Despite the arrays of drugs available in managing dementia, it appears no single drug can effectively treat dementia. Since it is multifactorial, combining potential drugs may provide neuroprotective impact. As such, this study investigated the neuroprotective effects of melatonin and vitamin C on scopolamine model of cognitive impairment in rats and the possible mechanism of action. Methods: Thirty male Wistar rats were divided to receive either normal saline (5 ml/kg, p.o), scopolamine (1 mg/kg, i.p.), donepezil (2 mg/kg, p.o), melatonin (10 mg/kg, p.o), vitamin C (100 mg/kg. p.o) or melatonin plus vitamin C. Cognitive impairment was induced by daily injection of scopolamine (1 mg/kg, i.p.), after which different treatment regimen were administered for 15 days. Spatial memory was assessed using Morris Water Maze and modified light and dark box. The brain was processed for malondialdehyde (MDA), reduced glutathione (GSH) and acetylcholinesterase (AchE) activity. Results: Scopolamine-treated rats with no intervention showed impaired learning and memory as depicted by a significant (p<0.05) increase in escape latency, reduction in the frequency of visit to the escape aperture, increased MDA, decreased GSH and elevated acetylcholinesterase activity when compared to other groups. Interventions with melatonin or/and vitamin C reversed these responses respectively. The melatonin plus vitamin C treated group compared favorably with donepezil (reference group). Conclusion: Melatonin and vitamin C show neuroprotective effect in attenuating cognitive impairment in scopolamine-induced model by modulating oxidative stress pathway and enhancing cholinergic neurotransmission.
  • Item
    Mercury chloride causes cognitive impairment, oxidative stress and neuroinflammation in male Wistar rats. The potential protective effect of 6-gingerol-rich fraction of Zingiber officinale via regulation of antioxidant defence system and reversal of pro-inflammatory markers increase.
    (Elsevier, 2024) Asuku, A.O.; Ayinla M.T; Ajibare, A.J.; Olajide T.S.
    This study investigated the effects of 6-gingerol-rich fraction of Zingiber officinale (6-GIRIFZO) on mercury chloride (HgCl2)-induced neurotoxicity in Wistar rats. Thirty -five male Wistar rats weighing between (150–200 g) were divided randomly into five groups (n = 7): group 1: control, received 0.5 mL of normal saline, group 2: received HgCl2 (5 mg/kg), group 3: received N-acetylcysteine (NAC) (50 mg/kg) as well as HgCl2 (5 mg/kg), group 4: received 6-GIRIFZO (100 mg/kg) and HgCl2 (5 mg/kg), group 5: had 6-GIRIFZO (200 mg/kg) and HgCl2 (5 mg/kg), consecutively for 14 days. On the day14, the rats were subjected to behavioural tests using a Morris water maze and novel object recognition tests. The rats were then euthanized to obtain brain samples for the determination of biochemical parameters (acetylcholinesterase (AchE), nitric oxide (NO), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), glutathione (GSH), tumor necrosis factor- alpha (TNF-α), nuclear factor kappa-B (NF-κB), interleukin-1β (IL-1β) and interleukin-6 (IL-6)) using standard methods. The result revealed a significant increase in escape latency and a significant decrease in recognition ratio in the rats that were exposed to HgCl2 only. However, 6-GIRIFZO produced a significant reduction in the escape latency and (p < 0.05) increase in the recognition ratio. Similarly, HgCl2 exposure caused a significant (p < 0.05) decrease in the brain SOD, GPx, CAT, GSH with increased brain levels of MDA, NO, AchE, TNF-α, NF-κB, IL-1β and IL-6. Similarly to the standard drug, NAC, 6-GIRIFZO (100 and 200 mg/kg) significantly (p < 0.05) increased brain SOD, GPx, CAT, and GSH levels with decreased concentrations of MDA, NO, AchE, TNF-α, NF-κB, IL-1β and IL-6. Also, pre-treatment with 6-GIRIFZO prevented the HgCl2-induced morphological aberrations in the rats. This study concludes that 6-GIRIFZO prevents HgCl2-induced cognitive deficit via reduction of brain inflammation as well as oxidative stress in rats.
  • Item
    Nutrition and Psychiatric Disorders: An Evidence-Based Approach to Understanding the Diet-Brain Connection
    (Springer Nature, Singapore, 2024) Asuku, A.O.; Ayinla M.T; Ajibare, A.J.
    Human eating habit is controlled by the central nervous system (CNS), a process that involves a plethora of molecular associations with numerous tissues, neurotransmitters, neural circuits, and hormones. It is governed by the hedonic and homeostatic systems interaction. Hedonic control is orchestrated through conscious and unconscious reward systems, whereas homeostatic control is governed by food- craving signals from the adipocytes, gut, as well as the vagus nerve. On the one hand, the CNS receives powerful food-related feedback via perception of texture, smell, sight, and taste, which in turn affects brain regions involved in reward pro- duced by feeding. Contrariwise, the nutrients essential in relatively large amounts for growth and health makeup increase the gut’s release of the hunger signal, which the central nervous system translates into unconsciously rewarding activities. This review considers how physiological impulses from the adipocytes, gastrointestinal tracts, and many more engage sets of interacting neural networks spread throughout the brain to bring about the complex motor occurrences that cause animals to eat in order to address the eating and brain functions by the central nervous system. Eating · Brain · Food · Central nervous system · Homeostatic system · Hedonic system
  • Item
    Nutrition and Psychiatric Disorders: An Evidence-Based Approach to Understanding the Diet-Brain Connection
    (Springer Nature, Singapore, 2024) Asuku, A.O.; Ayinla M.T; Ajibare, A.J.
    Abstract In nutrition research, mood is frequently measured, typically using rating scales. Positive mood encourages consumption, so it’s crucial to evaluate mood accurately. There is mounting proof that mood is influenced by nutritional elements such as high and less essential nutrients, such as vegetables, fruits, supplements, and eating habits. The purpose of this review is to take into account a variety of conven- tional and cutting-edge instruments for evaluating mood in relation to diet. We examine questionnaires that have been psychometrically validated to evaluate both specific moods (such as depression) and a variety of emotions (such as melancholy, anxiety, anger, and energy). We examine questionnaires that assess positive mood (such as vitality, happiness, and calmness), and we recommend that investigators should broaden their toolbox to encompass a wider scope of healthy indicators, such as gladness, eudaimonia, and satisfactory living, which is a good mood linked to meaning, engagement and purpose. The cutting-edge technological and method- ological aspects of real-time mood assessments were examined using experience sampling techniques, daily diaries, as well as ecological momentary evaluation, which are suitable for measuring moods as they happen on a daily or momentary basis, for instance, via smartphones’ use. We conclude by urging the incorporation of more cutting-edge platforms, with a focus on a variety of ambulatory techniques and sampling tactics. Real-time evaluation will continue to provide a scientifically sound method of evaluating the relationship between mood and food as it manifests in day-to-day living, opening our eyes to new possibilities.
  • Item
    The neurotoxic effects of lead acetate and the abrogating actions of 6-gingerol-rich extract of ginger via modulation of antioxidant defence system, pro-inflammatory markers, and apoptotic cascade
    (Springer on behalf of German Society of Experimental and Clinical Pharmacology and Toxicology (DGPT)., 2025) Ayinla M.T; Asuku, A.O.
    Lead exposure is a public health concern and it has been linked to cognitive deficit, memory impairment, and neurotoxicity. This study was designed to investigate the effect of 6-gingerol-rich extract of ginger (6-GREG) on oxidative stress, inflam- mation, and apoptosis in lead acetate (PbAc)-induced neurotoxicity in male Wistar rats. Twenty-five (25) male Wistar rats in total were divided into five groups at random (n = 5). The control group received 0.5 ml of normal saline, the PbAc-treated group received 7.5 mg/kg of PbAc, the vitamin C, 6-GREG (100), and 6-GREG (200) groups received 7.5 mg/kg of PbAc followed by administration of vitamin C (100 mg/kg), 6-GREG (100 mg/kg), and 6-GREG (200 mg/kg) respectively for 2 weeks. Following behavioral tests, the rats were euthanized, and their brain tissues were homogenized for biochemical analysis. When compared to the control group, the administration of PbAc caused behavioral alterations as well as a signifi- cant (p < 0.05) decrease in the activities of catalase, glutathione peroxidase, as well as reduced glutathione and Bcl-2 levels in the PbAc-treated group. Furthermore, the PbAc-treated group showed a statistically significant rise (p < 0.05) in brain acetylcholinesterase, malondialdehyde, nitric oxide, interleukin-1-beta, tumor necrosis factor-α, and caspase-9 levels in com- parison to the control. Administration of both 100 mg/kg and 200 mg/kg of 6-GREG effectively reversed these behavioral and biochemical changes in 6-GREG (100)- and 6-GREG (200)-treated groups respectively compared to the PbAc-treated group. Consequently, the study reveals the role of 6-GREG in attenuating PbAc-induced neurotoxicity and brain damage via antioxidative, anti-inflammatory, and anti-apoptotic mechanisms.
  • Item
    The neurotoxic effects of lead acetate and the abrogating actions of 6-gingerol-rich extract of ginger via modulation of antioxidant defence system, pro-inflammatory markers, and apoptotic cascade
    (published by Springer on behalf of German Society of Experimental and Clinical Pharmacology and Toxicology (DGPT), 2025) Ayinla M.T; Asuku, A.O.

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