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      Protective Effects of Tualang Honey against Oxidative Stress and Anxiety-Like Behaviour in Stressed Ovariectomized Rats

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          Abstract

          The present study aims to evaluate the antioxidant and anxiolytic-like effect of Tualang honey in stressed ovariectomized (OVX) rats. The animals were divided into; (i) nonstressed sham-operated control rats, (ii) sham-operated control rats exposed to stress, (iii) nonstressed OVX rats, (iv) OVX rats exposed to stress, (v) OVX rats exposed to stress and treated with 17 β-oestradiol (E2) (20  μg daily, sc), and (vi) OVX rats exposed to stress and treated with Tualang honey (0.2 g/kg body weight, orally). The open field test was used to evaluate the anxiety-like behaviour and ELISA kits were used to measure oxidant/antioxidant status of the brain homogenates. The result showed that anxiety-like behavior was significantly increased in stressed OVX compared to other groups, and administering either E2 or Tualang honey significantly decreased anxiety-like behaviour in stressed OVX rats. The levels of malondialdehyde (MDA) and protein carbonyl (PCO) were significantly decreased while the levels/activities of superoxide dismutase (SOD), glutathione S-transferases (GST), glutathione peroxidase (GPx), and glutathione reductase (GR) were significantly increased in the brain homogenates of treated stressed OVX groups compared to untreated stressed OVX. In conclusion, Tualang honey has protective effects against brain oxidative stress and may be useful alternative anxiolytic agent especially for postmenopausal women.

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          Most cited references71

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          Oxidative stress in anxiety and comorbid disorders.

          Anxiety disorders, depression, and alcohol use disorder are common neuropsychiatric diseases that often occur together. Oxidative stress has been suggested to contribute to their etiology. Oxidative stress is a consequence of either increased generation of reactive oxygen species or impaired enzymatic or non-enzymatic defense against it. When excessive it leads to damage of all major classes of macromolecules, and therefore affects several fundamentally important cellular functions. Consequences that are especially detrimental to the proper functioning of the brain include mitochondrial dysfunction, altered neuronal signaling, and inhibition of neurogenesis. Each of these can further contribute to increased oxidative stress, leading to additional burden to the brain. In this review, we will provide an overview of recent work on oxidative stress markers in human patients with anxiety, depressive, or alcohol use disorders, and in relevant animal models. In addition, putative oxidative stress-related mechanisms important for neuropsychiatric diseases are discussed. Despite the considerable interest this field has obtained, the detailed mechanisms that link oxidative stress to the pathogenesis of neuropsychiatric diseases remain largely unknown. Since this pathway may be amenable to pharmacological intervention, further studies are warranted. Copyright © 2010 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.
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            Oxidative stress and the pathogenesis of neurodegenerative disorders.

            Microglia-derived inflammatory neurotoxins play a principal role in the pathogenesis of neurodegenerative disorders including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and HIV-associated dementia; chief among these is reactive oxygen species. The detrimental effects of oxidative stress in the brain and nervous system are primarily a result of the diminished capacity of the central nervous system to prevent ongoing oxidative damage. A spectrum of environmental cues, mitochondrial dysfunction, accumulation of aberrant misfolded proteins, inflammation, and defects in protein clearance are known to evolve and form as a result of disease progression. These factors likely affect glial function serving to accelerate the tempo of disease. Understanding the relationships between disease progression, free radical formation, neuroinflammation, and neurotoxicity is critical to elucidating disease mechanisms and the development of therapeutic modalities to combat disease processes. In an era where populations continue to age, the prevalence and incidence of age-related neurodegenerative diseases are on the rise; therefore, the need for novel therapeutic strategies that attenuate neuroinflammation and protect neurons against oxidative stress is ever more immediate.
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              Effect of social isolation on stress-related behavioural and neuroendocrine state in the rat.

              The present study investigated the effects of post-weaning social isolation (SI) on behavioural and neuroendocrine reactivity to stress of male and female rats. Innate aspects of fear and anxiety were assessed in the open field and elevated plus maze tests. Spontaneous startle reflex and conditioned fear response were further investigated. The neuroendocrine response of isolates was examined by measuring basal and stress release of ACTH and corticosterone and by evaluating the mRNA expression of mineralocorticoid (MR) and glucocorticoid (GR) receptors using in situ hybridization. Locomotor activity in the open field was not modified by chronic SI. In males, but not females, SI produced an anxiogenic profile in the elevated plus maze. Male isolates showed a trend towards increased startle reflex amplitude relative to socially-reared controls. Moreover, SI in males produced alterations of the HPA axis functioning as reflected by higher basal levels of ACTH, and enhanced release of ACTH and corticosterone following stress. In contrast, startle response or HPA axis functioning were not altered in female isolates. Social isolates from both genders showed reduced contextual fear-conditioning. Finally, the mRNA expression of MR and GR was not modified by SI. The results of the present study suggest that chronic SI increases emotional reactivity to stress and produces a hyperfunction of the HPA axis in adult rats, particularly in males. Copyright 2003 Elsevier B.V.
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                Author and article information

                Journal
                Int Sch Res Notices
                Int Sch Res Notices
                ISRN
                International Scholarly Research Notices
                Hindawi Publishing Corporation
                2356-7872
                2014
                9 September 2014
                : 2014
                : 521065
                Affiliations
                1Institute of Health Sciences, Muscat, Ruwi, P.O. Box 3720, Code 112, Oman
                2Department of Physiology, School of Medical Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Malaysia
                3Department of Psychiatry, School of Medical Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Malaysia
                4Department of Anatomy, School of Medical Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Malaysia
                Author notes
                *Rahimah Zakaria: rahimah@ 123456usm.my

                Academic Editor: Fatima Martel

                Article
                10.1155/2014/521065
                4897279
                27379299
                90589078-d0c6-4023-962b-a3c06e1f0f79
                Copyright © 2014 Badriya Al-Rahbi et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 17 April 2014
                : 23 June 2014
                Categories
                Research Article

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