Please use this identifier to cite or link to this item: http://prr.hec.gov.pk/jspui/handle/123456789/17613
Title: Protective Effects of Coconut Oil and Nigella Sativa on Alcohol Induced Neurochemical and Behavioral Changes in Animal Model
Authors: Asrar, Beenish
Keywords: Biological & Medical Sciences
Biology
Issue Date: 2021
Publisher: International Islamic University, Islamabad.
Abstract: The neurological disorders represent the global health priority in terms of social and medical problems. Globally, the use of addictive substances or drugs is increasing day by day and roughly more than two billion people are using different drugs of abuse. Alcohol is one of the commonly available and used drugs of abuse regardless of knowing the facts of negative impacts on health. The chronic alcohol use in drinking water in animal model particularly in rats leads to the symptoms of anxiety, depression and cognitive impairments such as learning and memory. So, different approaches or neuroprotective strategies are adopted to overcome or reduce the negative consequences of alcohol on central nervous system. The aim and objectives of the current project were to evaluate the neuroprotective effects of Nigella sativa oil (NSO) and Virgin Cocos nucifera oil (VCO) in Wistar male rats of chronic alcohol consumption model. The total number of male rats (n=48) were divided in to two groups, a water drinking group and an ethanol drinking group. Each group was having 24 rats and then further divided into 4 groups having 6 rats each, i.e. two vehicle control groups (w) for Nigella sativa oil and (NSO) treated group and virgin coconut oil (VCO) treated group. Initially, the physical parameters such as body weight, food intake and fluid intake were measured in all groups. Rats were examined for anxiety by elevated plus maze test, spatial learning and memory by Morris water maze test, exploratory activity by open field test. Neurotransmitters like serotonin, dopamine, noradrenaline with their metabolite’s levels in prefrontal cortex, hippocampus and midbrain were measured by high pressure liquid chromatography- electrochemical detector. Furthermore, BDNF level in hypothalamus was evaluated by western blotting. Catalase enzyme and peroxide concentrations in striatum were evaluated by colorimetric assay. Concentrations of some of the important blood biomarkers such as serum glucose, total cholesterol and triglycerides were assessed by colorimeter/spectrophotometer and serum insulin was measured by Elisa. Our results showed that chronic alcohol reduced the body weight, food and fluid intake. NSO and VCO treatment of ethanol drinking animals exacerbated the effects of ethanol on body weight, food and fluid intake. VCO treatment also reduced food intake in water drinking animals. NSO significantly improved spatial memory and reduced anxiety in ethanolic rats where as VCO treatment led to anxiety in water and ethanol drinking rats but xii significantly improved memory in water drinking group only. Brain serotonin and its metabolite concentrations were elevated in NSO treated water and ethanolic rats whereas prefrontal serotonin (5-HT) and its metabolite “5-HIAA” levels were increased by VCO treatment in water drinking animals only. Brain 5-HT level was reduced in VCO treated ethanolic rats. Brain dopamine (DA) metabolism was enhanced caused increase in DA’s metabolite “DOPAC” level in water and ethanol drinking rats treated with NSO. VCO treatment led to reduced prefrontal DA levels in water and ethanolic rats and increased DOPAC level only in water drinking animals. NSO treated water drinking rats showed reduced hippocampal noradrenaline and serum glucose whereas results were vice versa for VCO treated water drinking rats but VCO acted as hypoglycemic agent in the ethanolic rats. NSO and VCO treated groups showed reduced total cholesterol in ethanol drinking group. Triglycerides level was increased in VCO treated water and ethanolic rats. The present studies provide enough evidence that chronic alcohol leads to memory impairment, anxiety with impaired neurotransmission. In conclusion, this study has provided enough evidences that chronic alcohol leads to anxiety and impaired memory by altered neurotransmission. The findings of this study also explored that NSO counteracts the impaired memory, anxiogenic effects of chronic ethanol by improving the 5-HT and DA neurotransmission. VCO can be useful to improve memory in water drinking animals only by increased prefrontal serotonin and noradrenalin levels. Ethanol drinking rats treated with VCO showed anxiety and impaired memory with reduced serotonin, dopamine and DOPAC. In future, the active compounds from VCO and NSO will be tested on same parameters tested and would aid knowledge to scientific world.
Gov't Doc #: 23730
URI: http://prr.hec.gov.pk/jspui/handle/123456789/17613
Appears in Collections:PhD Thesis of All Public / Private Sector Universities / DAIs.

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