Walnut supplementation reverses the scopolamine-induced memory impairment by restoration of cholinergic function via mitigating oxidative stress in rats: a potential therapeutic intervention for age related neurodegenerative disorders

被引:0
作者
Saida Haider
Zehra Batool
Saara Ahmad
Rafat Ali Siddiqui
Darakhshan Jabeen Haleem
机构
[1] University of Karachi,Neurochemistry and Biochemical Neuropharmacology Research Unit, Department of Biochemistry
[2] The Aga Khan University,Department of Biological and Biomedical Sciences
[3] Virginia State University,Food Chemistry and Nutrition Science Laboratory
[4] University of Karachi,Neuroscience Research Laboratory, Dr Panjwani Center for Molecular Medicine and Drug Research
来源
Metabolic Brain Disease | 2018年 / 33卷
关键词
Acetylcholine; Acetylcholinesterase; Memory; Oxidative stress; Scopolamine; Walnut;
D O I
暂无
中图分类号
学科分类号
摘要
The brain is highly susceptible to the damaging effects of oxidative reactive species. The free radicals which are produced as a consequence of aerobic respiration can cause cumulative oxygen damage which may lead to age-related neurodegeneration. Scopolamine, the anti-muscarinic agent, induces amnesia and oxidative stress similar to that observed in the older age. Studies suggest that antioxidants derived from plant products may provide protection against oxidative stress. Therefore, the present study was designed to investigate the attenuation of scopolamine-induced memory impairment and oxidative stress by walnut supplementation in rats. Rats in test group were administrated with walnut suspension (400 mg/kg/day) for four weeks. Both control and walnut-treated rats were then divided into saline and scopolamine-treated groups. Rats in the scopolamine group were injected with scopolamine (0.5 mg/kg dissolved in saline) five minutes before the start of each memory test. Memory was assessed by elevated plus maze (EPM), Morris water maze (MWM), and novel object recognition task (NOR) followed by estimation of regional acetylcholine levels and acetylcholinesterase activity. In the next phase, brain oxidative status was determined by assaying lipid peroxidation, and measuring superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) activities. Results showed that scopolamine-treatment impaired memory function, caused cholinergic dysfunction, and induced oxidative stress in rats compared to that saline-treated controls. These impairments were significantly restored by pre-administration of walnut. This study demonstrates that antioxidant properties of walnut may provide augmented effects on cholinergic function by reducing oxidative stress and thus improving memory performance.
引用
收藏
页码:39 / 51
页数:12
相关论文
共 318 条
  • [1] Albright CD(1999)Maternal dietary choline availability alters mitosis, apoptosis and the localization of TOAD-64 protein in the developing fetal rat septum Brain Res Dev Brain Res 115 123-129
  • [2] Friedrich CB(1999)Choline availability alters embryonic development of the hippocampus and septum in the rat Brain Res Dev Brain Res 113 13-20
  • [3] Brown EC(2012)Ionizing radiation-induce metabolic oxidative stress and prolonged cell injury Cancer Lett 327 48-60
  • [4] Mar MH(2004)Oral choline increases choline metabolites in human brain Psychiatry Res 130 1-9
  • [5] Zeisel SH(2009)Effects of walnut consumption on blood lipids and other cardiovascular risk factors: a meta-analysis and systematic review Am J Clin Nutr 90 56-63
  • [6] Albright CD(2016)Repeated administration of almonds increases brain acetylcholine levels and enhances memory function in healthy rats while attenuates memory deficits in animal model of amnesia Brain Res Bull 120 63-74
  • [7] Tsai AY(2017)Role of oxidative stress and antioxidants in daily nutrition and human health Nutrition 33 311-321
  • [8] Friedrich CB(2005)Dietary antioxidants and cardiovascular disease Curr Opin Lipidol 16 47-54
  • [9] Mar MH(2010)Oxidative stress in Alzheimer disease: a possibility for prevention Neuropharmacology 59 290-294
  • [10] Zeisel SH(2006)Nuts: source of energy and macronutrients Br J Nutr 96 24-28