All Title Author
Keywords Abstract


Effect of Resveratrol as Caloric Restriction Mimetic and Environmental Enrichment on Neurobehavioural Responses in Young Healthy Mice

DOI: 10.1155/2014/545170

Full-Text   Cite this paper   Add to My Lib

Abstract:

Caloric restriction and environmental enrichment have been separately reported to possess health benefits such as improvement in motor and cognitive functions. Resveratrol, a natural polyphenolic compound, has been reported to be caloric restriction mimetic. This study therefore aims to investigate the potential benefit of the combination of resveratrol as CR and EE on learning and memory, motor coordination, and motor endurance in young healthy mice. Fifty mice of both sexes were randomly divided into five groups of 10 animals each: group I animals received carboxymethylcellulose (CMC) orally per kg/day (control), group II animals were maintained on every other day feeding, group III animals received resveratrol 50?mg/kg, suspended in 10?g/L of (CMC) orally per kg/day, group IV animals received CMC and were kept in an enriched environment, and group V animals received resveratrol 50?mg/kg and were kept in EE. The treatment lasted for four weeks. On days 26, 27, and 28 of the study period, the animals were subjected to neurobehavioural evaluation. The results obtained showed that there was no significant change in neurobehavioural responses in all the groups when compared to the control which indicates that 50?mg/kg of resveratrol administration and EE have no significant effects on neurobehavioural responses in young healthy mice over a period of four weeks. 1. Introduction Dietary restriction (DR), otherwise known as caloric restriction (CR), has been generally defined as consumption of nutritious diet that is 30% to 40% less in calories compared to ad libitum diet [1]. In other words, CR can be defined as a simple reduction in caloric intake in the absence of malnutrition [2]. Caloric restriction has been demonstrated to possess many health benefits. It provides protection against numerous deadly diseases such as cancer, neurological disorders, and obesity and is found to be the only reliable treatment that extends lifespan or causes healthy aging consistently in a multitude of organisms ranging from bacteria to monkeys [3–5]. The most frequently mentioned effect of CR has been its influence on creating a mild stress in the organism and a typical upregulation of adaptive mechanisms involving stress proteins accompanied by elevated defence or survival molecules [6]. Caloric restriction (CR) has also been found to retard several aspects of the aging process in mammals, including age-related mortality, tumorigenesis, physiological decline [7], and the establishment of age-related transcriptional profiles [8]. Resveratrol (3,5′,4-trihydroxystilbene), a

References

[1]  T. S. Anekonda, “The benefits of caloric restriction and caloric restriction mimetics as related to the eye,” Open Longevity Science, vol. 3, pp. 28–37, 2009.
[2]  J. A. Baur, K. J. Pearson, N. L. Price et al., “Resveratrol improves health and survival of mice on a high-calorie diet,” Nature, vol. 444, no. 7117, pp. 337–342, 2006.
[3]  M. Obin, A. Pike, M. Halbleib, R. Lipman, A. Taylor, and R. Bronson, “Calorie restriction modulates age-dependent changes in the retinas of Brown Norway rats,” Mechanisms of Ageing and Development, vol. 114, no. 2, pp. 133–147, 2000.
[4]  S. Lin, E. Ford, M. Haigis, G. Liszt, and L. Guarente, “Calorie restriction extends yeast life span by lowering the level of NADH,” Genes and Development, vol. 18, no. 1, pp. 12–16, 2004.
[5]  G. Wolf, “Calorie restriction increases life span: a molecular mechanism,” Nutrition Reviews, vol. 64, no. 2, pp. 89–92, 2006.
[6]  D. A. Sinclair, “Toward a unified theory of caloric restriction and longevity regulation,” Mechanisms of Ageing and Development, vol. 126, no. 9, pp. 987–1002, 2005.
[7]  R. Weindruch and R. L. Walford, The Retardation of Aging and Disease by Dietary Restriction, Charles C. Thomas, Springfield, Ill, USA, 1988.
[8]  C.-K. Lee, R. G. Klopp, R. Weindruch, and T. A. Prolla, “Gene expression profile of aging and its retardation by caloric restriction,” Science, vol. 285, no. 5432, pp. 1390–1393, 1999.
[9]  K. T. Howitz, K. J. Bitterman, H. Y. Cohen et al., “Small molecule activators of sirtuins extend Saccharomyces cerevisiae lifespan,” Nature, vol. 425, no. 6954, pp. 191–196, 2003.
[10]  J. H. Bauer, S. Goupil, G. B. Garber, and S. L. Helfand, “An accelerated assay for the identification of lifespan-extending interventions in Drosophila melanogaster,” Proceedings of the National Academy of Sciences of the United States of America, vol. 101, no. 35, pp. 12980–12985, 2004.
[11]  J. G. Wood, B. Rogina, S. Lavu et al., “Sirtuin activators mimic caloric restriction and delay ageing in metazoans,” Nature, vol. 430, no. 7000, pp. 686–689, 2004.
[12]  M. Viswanathan, S. K. Kim, A. Berdichevsky, and L. Guarente, “A role for SIR-2.1 regulation of ER stress response genes in determining C. elegans life span,” Developmental Cell, vol. 9, no. 5, pp. 605–615, 2005.
[13]  D. R. Valenzano, E. Terzibasi, T. Genade, A. Cattaneo, L. Domenici, and A. Cellerino, “Resveratrol prolongs lifespan and retards the onset of age-related markers in a short-lived vertebrate,” Current Biology, vol. 16, no. 3, pp. 296–300, 2006.
[14]  M. Lagouge, C. Argmann, Z. Gerhart-Hines et al., “Resveratrol improves mitochondrial function and protects against metabolic disease by activating SIRT1 and PGC-1alpha,” Cell, vol. 127, no. 6, pp. 1109–1122, 2006.
[15]  A. Anastasía, L. Torre, G. A. de Erausquin, and D. H. Mascó, “Enriched environment protects the nigrostriatal dopaminergic system and induces astroglial reaction in the 6-OHDA rat model of Parkinson's disease,” Journal of Neurochemistry, vol. 109, no. 3, pp. 755–765, 2009.
[16]  J. Nithianantharajah and A. J. Hannan, “Enriched environments, experience-dependent plasticity and disorders of the nervous system,” Nature Reviews Neuroscience, vol. 7, no. 9, pp. 697–709, 2006.
[17]  G. Laviola, A. J. Hannan, S. Macrì, M. Solinas, and M. Jaber, “Effects of enriched environment on animal models of neurodegenerative diseases and psychiatric disorders,” Neurobiology of Disease, vol. 31, no. 2, pp. 159–168, 2008.
[18]  E. Bezard, S. Dovero, D. Belin et al., “Enriched environment confers resistance to 1-methyl-4-phenyl-1 ,2,3,6 -tetrahydropyridine and cocaine: involvement of dopamine transporter and trophic factors,” Journal of Neuroscience, vol. 23, no. 35, pp. 10999–11007, 2003.
[19]  C. J. Faherty, K. R. Shepherd, A. Herasimtschuk, and R. J. Smeyne, “Environmental enrichment in adulthood eliminates neuronal death in experimental Parkinsonism,” Molecular Brain Research, vol. 134, no. 1, pp. 170–179, 2005.
[20]  N. M. Jadavji, B. Kolb, and G. A. Metz, “Enriched environment improves motor function in intact and unilateral dopamine-depleted rats,” Neuroscience, vol. 140, no. 4, pp. 1127–1138, 2006.
[21]  B. R. Ickes, T. M. Pham, L. A. Sanders, D. S. Albeck, A. H. Mohammed, and A. Granholm, “Long-term environmental enrichment leads to regional increases in neurotrophin levels in rat brain,” Experimental Neurology, vol. 164, no. 1, pp. 45–52, 2000.
[22]  T. L. Spires, H. E. Grote, N. K. Varshney et al., “Environmental enrichment rescues protein deficits in a mouse model of Huntington’s disease, indicating a possible disease mechanism,” Journal of Neuroscience, vol. 24, no. 9, pp. 2270–2276, 2004.
[23]  B. Steiner, C. Winter, K. Hosman et al., “Enriched environment induces cellular plasticity in the adult substantia nigra and improves motor behavior function in the 6-OHDA rat model of Parkinson's disease,” Experimental Neurology, vol. 199, no. 2, pp. 291–300, 2006.
[24]  J. A. Baur, “Resveratrol, sirtuins, and the promise of a DR mimetic,” Mechanisms of Ageing and Development, vol. 131, no. 4, pp. 261–269, 2010.
[25]  D. Kim, M. D. Nguyen, M. M. Dobbin et al., “SIRT1 deacetylase protects against neurodegeneration in models for Alzheimer's disease and amyotrophic lateral sclerosis,” The EMBO Journal, vol. 26, no. 13, pp. 3169–3179, 2007.
[26]  L. Deng, Z.-N. Wu, and P.-Z. Han, “Effects of different levels of food restriction on passive-avoidance memory and the expression of synapsin I in young mice,” International Journal of Neuroscience, vol. 119, no. 2, pp. 291–304, 2009.
[27]  T. Hashimoto and S. Watanabe, “Chronic food restriction enhances memory in mice-analysis with matched drive levels,” NeuroReport, vol. 16, no. 10, pp. 1129–1133, 2005.
[28]  S. Yanai, Y. Okaichi, and H. Okaichi, “Long-term dietary restriction causes negative effects on cognitive functions in rats,” Neurobiology of Aging, vol. 25, no. 3, pp. 325–332, 2004.
[29]  L. L. Harburger, T. J. Lambert, and K. M. Frick, “Age-dependent effects of environmental enrichment on spatial reference memory in male mice,” Behavioural Brain Research, vol. 185, no. 1, pp. 43–48, 2007.
[30]  M. P. Mattson, W. Duan, J. Lee, and Z. Guo, “Suppression of brain aging and neurodegenerative disorders by dietary restriction and environmental enrichment: molecular mechanisms,” Mechanisms of Ageing and Development, vol. 122, no. 7, pp. 757–778, 2001.
[31]  M. E., lia Juan, M. Pilar Vinardell, and J. M. Planas, “The daily oral administration of high doses of trans-resveratrol to rats for 28 days is not harmful,” Journal of Nutrition, vol. 132, no. 2, pp. 257–260, 2002.
[32]  J. Blanchet, F. Longpré, G. Bureau et al., “Resveratrol, a red wine polyphenol, protects dopaminergic neurons in MPTP-treated mice,” Progress in Neuro-Psychopharmacology and Biological Psychiatry, vol. 32, no. 5, pp. 1243–1250, 2008.
[33]  J. L. Stanley, R. J. Lincoln, T. A. Brown, L. M. McDonald, G. R. Dawson, and D. S. Reynolds, “The mouse beam walking assay offers improved sensitivity over the mouse rotarod in determining motor coordination deficits induced by benzodiazepines,” Journal of Psychopharmacology, vol. 19, no. 3, pp. 221–227, 2005.
[34]  M. Mohanasundari, M. S. Srinivasan, S. Sethupathy, and M. Sabesan, “Enhanced neuroprotective effect by combination of bromocriptine and Hypericum perforatum extract against MPTP-induced neurotoxicity in mice,” Journal of the Neurological Sciences, vol. 249, no. 2, pp. 140–144, 2006.
[35]  J. L. Tillerson, W. M. Caudle, M. E. Reverón, and G. W. Miller, “Detection of behavioral impairments correlated to neurochemical deficits in mice treated with moderate doses of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine,” Experimental Neurology, vol. 178, no. 1, pp. 80–90, 2002.
[36]  J. Itoh, T. Nabeshima, and T. Kameyama, “Utility of an elevated plus-maze for the evaluation of memory in mice: effects of nootropics, scopolamine and electroconvulsive shock,” Psychopharmacology, vol. 101, no. 1, pp. 27–33, 1990.
[37]  A. Anandhan, K. Tamilselvam, D. Vijayranjah, N. Ashokkumar, S. Rajasankar, and T. Manivasagam, “Resveratrol attenuate oxidative stress and improves behaviour in 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) challenged mice,” Annals of Neuroscience, vol. 17, no. 3, pp. 113–119, 2010.
[38]  J. Long, H. Gao, L. Sun, J. Liu, and X. Zhao-Wilson, “Grape extract protects mitochondria from oxidative damage and improves locomotor dysfunction and extends lifespan in a drosophila parkinson's disease model,” Rejuvenation Research, vol. 12, no. 5, pp. 321–331, 2009.
[39]  R. Takahashi, Y. Komiya, and S. Goto, “Effect of dietary restriction on learning and memory impairment and histologic alterations of brain stem in senescence-accelerated mouse (SAM) P8 strain,” Annals of the New York Academy of Sciences, vol. 1067, no. 1, pp. 388–393, 2006.
[40]  W. Duan, Z. Guo, and M. P. Mattson, “Brain-derived neurotrophic factor mediates an excitoprotective effect of dietary restriction in mice,” Journal of Neurochemistry, vol. 76, no. 2, pp. 619–626, 2001.
[41]  A. Wu, X. Sun, and Y. Liu, “Effects of caloric restriction on cognition and behavior in developing mice,” Neuroscience Letters, vol. 339, no. 2, pp. 166–168, 2003.
[42]  M. C. Roberge, J. Hotte-Bernard, C. Messier, and H. Plamondon, “Food restriction attenuates ischemia-induced spatial learning and memory deficits despite extensive CA1 ischemic injury,” Behavioural Brain Research, vol. 187, no. 1, pp. 123–132, 2008.
[43]  V. Tucci, A. Hardy, and P. M. Nolan, “A comparison of physiological and behavioural parameters in C57BL/6J mice undergoing food or water restriction regimes,” Behavioural Brain Research, vol. 173, no. 1, pp. 22–29, 2006.
[44]  M. M. Story, J. S. Rand, M. Shyan-Norwalt, R. Mesch, J. M. Morton, and E. A. Flickinger, “Effect of resveratrol supplementation on the performance of dogs in an eight-arm radial maze,” The Open Nutrition Journal, vol. 6, pp. 80–88, 2012.
[45]  M. K. Shigenaga, T. M. Hagen, and B. N. Ames, “Oxidative damage and mitochondrial decay in aging,” Proceedings of the National Academy of Sciences of the United States of America, vol. 91, no. 23, pp. 10771–10778, 1994.
[46]  E. Head, J. Liu, T. M. Hagen et al., “Oxidative damage increases with age in a canine model of human brain aging,” Journal of Neurochemistry, vol. 82, no. 2, pp. 375–381, 2002.
[47]  P. D. Tapp, C. T. Siwak, F. Q. Gao et al., “Frontal lobe volume, function, and β-amyloid pathology in a canine model of aging,” The Journal of Neuroscience, vol. 24, no. 38, pp. 8205–8213, 2004.
[48]  C. T. Siwak-Tapp, E. Head, B. A. Muggenburg, N. W. Milgram, and C. W. Cotman, “Region specific neuron loss in the aged canine hippocampus is reduced by enrichment,” Neurobiology of Aging, vol. 29, no. 1, pp. 39–50, 2008.
[49]  K. J. Pearson, J. A. Baur, K. N. Lewis et al., “Resveratrol delays age-related deterioration and mimics transcriptional aspects of dietary restriction without extending life span,” Cell Metabolism, vol. 8, no. 2, pp. 157–168, 2008.
[50]  M. Sharma and Y. K. Gupta, “Chronic treatment with trans resveratrol prevents intracerebroventricular streptozotocin induced cognitive impairment and oxidative stress in rats,” Life Sciences, vol. 71, no. 21, pp. 2489–2498, 2002.
[51]  ü. S?nmez, A. S?nmez, G. Erbil, I. Tekmen, and B. Baykara, “Neuroprotective effects of resveratrol against traumatic brain injury in immature rats,” Neuroscience Letters, vol. 420, no. 2, pp. 133–137, 2007.
[52]  J. L. Bowers, V. V. Tyulmenkov, S. C. Jernigan, and C. M. Klinge, “Resveratrol acts as a mixed agonist/antagonist for estrogen receptors α and β,” Endocrinology, vol. 141, no. 10, pp. 3657–3667, 2000.
[53]  J. E. Gresack and K. M. Frick, “Environmental enrichment reduces the mnemonic and neural benefits of estrogen,” Neuroscience, vol. 128, no. 3, pp. 459–471, 2004.
[54]  J. E. Gresack, K. M. Kerr, and K. M. Frick, “Short-term environmental enrichment decreases the mnemonic response to estrogen in young, but not aged, female mice,” Brain Research, vol. 1160, no. 1, pp. 91–101, 2007.
[55]  J. Bohacek and J. M. Daniel, “Increased daily handling of ovariectomized rats enhances performance on a radial-maze task and obscures effects of estradiol replacement,” Hormones and Behavior, vol. 52, no. 2, pp. 237–243, 2007.
[56]  J. M. Levenson, K. J. O'Riordan, K. D. Brown, M. A. Trinh, D. L. Molfese, and J. D. Sweatt, “Regulation of histone acetylation during memory formation in the hippocampus,” The Journal of Biological Chemistry, vol. 279, no. 39, pp. 40545–40559, 2004.
[57]  W. B. Chwang, J. S. Arthur, A. Schumacher, and J. D. Sweatt, “The nuclear kinase mitogen- and stress-activated protein kinase 1 regulates hippocampal chromatin remodeling in memory formation,” The Journal of Neuroscience, vol. 27, no. 46, pp. 12732–12742, 2007.
[58]  A. Fischer, F. Sananbenesi, X. Wang, M. Dobbin, and L. Tsai, “Recovery of learning and memory is associated with chromatin remodelling,” Nature, vol. 447, no. 7141, pp. 178–182, 2007.
[59]  T. Abel and R. S. Zukin, “Epigenetic targets of HDAC inhibition in neurodegenerative and psychiatric disorders,” Current Opinion in Pharmacology, vol. 8, no. 1, pp. 57–64, 2008.
[60]  L. Guarente and F. Picard, “Calorie restriction—the SIR2 connection,” Cell, vol. 120, no. 4, pp. 473–482, 2005.
[61]  M. S. Finnin, J. R. Donigian, A. Cohen et al., “Structures of a histone deacetylase homologue bound to the TSA and SAHA inhibitors,” Nature, vol. 401, no. 6749, pp. 188–193, 1999.
[62]  J. J. Buggy, M. L. Sideris, P. Mak, D. D. Lorimer, B. McIntosh, and J. M. Clark, “Cloning and characterization of a novel human histone deacetylase, HDAC8,” Biochemical Journal, vol. 350, no. 1, pp. 199–205, 2000.
[63]  J. D. Sweatt, “Experience-dependent epigenetic modifications in the central nervous system,” Biological Psychiatry, vol. 65, no. 3, pp. 191–197, 2009.

Full-Text

comments powered by Disqus

Contact Us

service@oalib.com

QQ:3279437679

微信:OALib Journal