Neuroprotective effect of virgin coconut oil on lipopoly saccharide-induced cell death in SK-N-SH and memory impairment in rat / Nur Syafiqah Rahim

Neuroprotective effect of virgin coconut oil on lipopoly saccharide-induced cell death in SK-N-SH and memory impairment in rat / Nur Syafiqah Rahim

Neuroinflammation has been implicated in the pathogenesis of Alzheimer’s Disease (AD) and often characterized by activation of glial cells and the subsequent upregulation of various cytokines. Neuronal damage would then set in and lead to deterioration of cognitive function. Virgin Coconut Oil (VCO)...

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Main Author: Rahim, Nur Syafiqah
Format: Thesis
Language:English
Published: 2015
Subjects:
Biochemistry
Online Access:https://ir.uitm.edu.my/id/eprint/15910/2/15910.pdf
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spelling my-uitm-ir.159102022-11-24T03:56:31Z Neuroprotective effect of virgin coconut oil on lipopoly saccharide-induced cell death in SK-N-SH and memory impairment in rat / Nur Syafiqah Rahim 2015 Rahim, Nur Syafiqah Biochemistry Pharmacognosy. Pharmaceutical substances (Plant, animal, and inorganic) Neuroinflammation has been implicated in the pathogenesis of Alzheimer’s Disease (AD) and often characterized by activation of glial cells and the subsequent upregulation of various cytokines. Neuronal damage would then set in and lead to deterioration of cognitive function. Virgin Coconut Oil (VCO) has been reported to possess anti-bacterial, anti-viral, anti-oxidants and anti-inflammatory properties. Capitalizing on these therapeutic effects, the present study investigated for the first time the potential neuroprotective effect of VCO in vitro and in vivo. For this purpose, neuroprotection by VCO against amyloid-/3-(A/3) and Lipopolysaccharide(LPS)- induced cell death and Reactive Oxygen Species (ROS) production of SK-N-SH (neuroblastoma cells) was assessed. The in vitro findings were validated using normal and LPS-induced memory impaired animal models in vivo. A total of 36 male Wistar rats (7-8 weeks) were randomly assigned to 6 groups (n=6/group). The treatment groups were administered with 1, 5 and lOmL/kg of VCO for 31 days by oral gavages. The cognitive functions of the treated-rats were then assessed using the Morris Water Maze Test. Collected brains were homogenised and subjected to biochemical analyses of Acetylcholine (ACh), Acetylcholinesterase (AChE), antioxidative enzymes [Superoxide dismutase (SOD), Catalase (CAT), Glutathione (GSH), Glutathione peroxidase (GPx) and Glutathione reductase (GRx)], lipid peroxidase [Malondialdehyde (MDA)], nitric oxide (NO), cytokines (IL1-/3, IFN-y and IL-10) as well as inflammatory (COX-2 and iNOS) and amyloidogenic genes (BACE-1). Next, yet another 48 male Wistar rats (7-8 weeks) were assigned for neuroinflammatory study. The treatment groups (1, 5 and lOml/kg) were administered with 1, 5 and 1 OmL/kg of VCO for 31 days by oral gavage in the presence of 0.25 mg/kg LPS (i.p.). a-Tocopherol (150 mg/kg) was used as positive control throughout the in vivo studies. The results showed that 100|ag/mL VCO significantly improved viability of SK-N-SH (+47.25%; p<0.01 and 57.46%; p<0.001) and inhibited ROS production (-18.36%; p<0.001 and -30.96%; p<0.001) in the presence of A/3 and LPS respectively. Subsequent validation in normal rats indicated that VCO significantly enhanced cognitive functions [escape latency (-29.62±1.22%), escape distance (-23.87±0.20%) and total time spent on platform (+36.84%; p<0.05)]. The findings were mediated through elevation of ACh (+15.39%; p<0.001), SOD (+8.30%; p<0.05), CAT (+67.15%; p<0.001), GSH (+30.45%; p<0.001) and GPx (+14.31%; p<0.001) and reduction of AChE (-23.16%; p<0.001), MDA (-45.14%; p<0.001) and NO (-65.38%; p<0.001). On the other hand, exposure of LPS-induced memory impaired rats to VCO resulted significantly improved cognitive functions [escape latency(-45.87±0.61%), escape distance (-32.63+0.24%) and total time spent on platform (+81.82%; p<0.01)].The improvements were mediated through elevation of ACh (+26.80%; p<0.001), SOD (+8.25%; p<0.05), CAT (+69.50%; p<0.001), GSH (+99.27%; p<0.001), GPx (+15.10%; p<0.001), GRx (+26.40%; p<0.001) and IL-10 (+34.05%; p<0.01) and reduction of AChE (-44.83%; p<0.001), MDA (-58.73%; p<0.001), NO (-52.71%; p<0.001), IL-10 (-64.85%; p<0.001), IFN-y (-25.03%; p<0.05), COX-2 (-67.73%; p<0.001), iNOS (-65.63%; p<0.001) and BACE-1 (-75%; p<0.001). The present findings strongly implied that VCO has neuroprotective effects and has the potential to be a memory enhancer. This neuroprotective effect was mediated, at least in part, through the inflammatory, cholinergic and amyloidogenic pathways. 2015 Thesis https://ir.uitm.edu.my/id/eprint/15910/ https://ir.uitm.edu.my/id/eprint/15910/2/15910.pdf text en public mphil masters Universiti Teknologi MARA Faculty of Pharmacy
institution Universiti Teknologi MARA
collection UiTM Institutional Repository
language English
topic Biochemistry
Biochemistry
spellingShingle Biochemistry
Biochemistry
Rahim, Nur Syafiqah
Neuroprotective effect of virgin coconut oil on lipopoly saccharide-induced cell death in SK-N-SH and memory impairment in rat / Nur Syafiqah Rahim
description Neuroinflammation has been implicated in the pathogenesis of Alzheimer’s Disease (AD) and often characterized by activation of glial cells and the subsequent upregulation of various cytokines. Neuronal damage would then set in and lead to deterioration of cognitive function. Virgin Coconut Oil (VCO) has been reported to possess anti-bacterial, anti-viral, anti-oxidants and anti-inflammatory properties. Capitalizing on these therapeutic effects, the present study investigated for the first time the potential neuroprotective effect of VCO in vitro and in vivo. For this purpose, neuroprotection by VCO against amyloid-/3-(A/3) and Lipopolysaccharide(LPS)- induced cell death and Reactive Oxygen Species (ROS) production of SK-N-SH (neuroblastoma cells) was assessed. The in vitro findings were validated using normal and LPS-induced memory impaired animal models in vivo. A total of 36 male Wistar rats (7-8 weeks) were randomly assigned to 6 groups (n=6/group). The treatment groups were administered with 1, 5 and lOmL/kg of VCO for 31 days by oral gavages. The cognitive functions of the treated-rats were then assessed using the Morris Water Maze Test. Collected brains were homogenised and subjected to biochemical analyses of Acetylcholine (ACh), Acetylcholinesterase (AChE), antioxidative enzymes [Superoxide dismutase (SOD), Catalase (CAT), Glutathione (GSH), Glutathione peroxidase (GPx) and Glutathione reductase (GRx)], lipid peroxidase [Malondialdehyde (MDA)], nitric oxide (NO), cytokines (IL1-/3, IFN-y and IL-10) as well as inflammatory (COX-2 and iNOS) and amyloidogenic genes (BACE-1). Next, yet another 48 male Wistar rats (7-8 weeks) were assigned for neuroinflammatory study. The treatment groups (1, 5 and lOml/kg) were administered with 1, 5 and 1 OmL/kg of VCO for 31 days by oral gavage in the presence of 0.25 mg/kg LPS (i.p.). a-Tocopherol (150 mg/kg) was used as positive control throughout the in vivo studies. The results showed that 100|ag/mL VCO significantly improved viability of SK-N-SH (+47.25%; p<0.01 and 57.46%; p<0.001) and inhibited ROS production (-18.36%; p<0.001 and -30.96%; p<0.001) in the presence of A/3 and LPS respectively. Subsequent validation in normal rats indicated that VCO significantly enhanced cognitive functions [escape latency (-29.62±1.22%), escape distance (-23.87±0.20%) and total time spent on platform (+36.84%; p<0.05)]. The findings were mediated through elevation of ACh (+15.39%; p<0.001), SOD (+8.30%; p<0.05), CAT (+67.15%; p<0.001), GSH (+30.45%; p<0.001) and GPx (+14.31%; p<0.001) and reduction of AChE (-23.16%; p<0.001), MDA (-45.14%; p<0.001) and NO (-65.38%; p<0.001). On the other hand, exposure of LPS-induced memory impaired rats to VCO resulted significantly improved cognitive functions [escape latency(-45.87±0.61%), escape distance (-32.63+0.24%) and total time spent on platform (+81.82%; p<0.01)].The improvements were mediated through elevation of ACh (+26.80%; p<0.001), SOD (+8.25%; p<0.05), CAT (+69.50%; p<0.001), GSH (+99.27%; p<0.001), GPx (+15.10%; p<0.001), GRx (+26.40%; p<0.001) and IL-10 (+34.05%; p<0.01) and reduction of AChE (-44.83%; p<0.001), MDA (-58.73%; p<0.001), NO (-52.71%; p<0.001), IL-10 (-64.85%; p<0.001), IFN-y (-25.03%; p<0.05), COX-2 (-67.73%; p<0.001), iNOS (-65.63%; p<0.001) and BACE-1 (-75%; p<0.001). The present findings strongly implied that VCO has neuroprotective effects and has the potential to be a memory enhancer. This neuroprotective effect was mediated, at least in part, through the inflammatory, cholinergic and amyloidogenic pathways.
format Thesis
qualification_name Master of Philosophy (M.Phil.)
qualification_level Master's degree
author Rahim, Nur Syafiqah
author_facet Rahim, Nur Syafiqah
author_sort Rahim, Nur Syafiqah
title Neuroprotective effect of virgin coconut oil on lipopoly saccharide-induced cell death in SK-N-SH and memory impairment in rat / Nur Syafiqah Rahim
title_short Neuroprotective effect of virgin coconut oil on lipopoly saccharide-induced cell death in SK-N-SH and memory impairment in rat / Nur Syafiqah Rahim
title_full Neuroprotective effect of virgin coconut oil on lipopoly saccharide-induced cell death in SK-N-SH and memory impairment in rat / Nur Syafiqah Rahim
title_fullStr Neuroprotective effect of virgin coconut oil on lipopoly saccharide-induced cell death in SK-N-SH and memory impairment in rat / Nur Syafiqah Rahim
title_full_unstemmed Neuroprotective effect of virgin coconut oil on lipopoly saccharide-induced cell death in SK-N-SH and memory impairment in rat / Nur Syafiqah Rahim
title_sort neuroprotective effect of virgin coconut oil on lipopoly saccharide-induced cell death in sk-n-sh and memory impairment in rat / nur syafiqah rahim
granting_institution Universiti Teknologi MARA
granting_department Faculty of Pharmacy
publishDate 2015
url https://ir.uitm.edu.my/id/eprint/15910/2/15910.pdf
_version_ 1783733466122158080

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