Reviews

Hormesis and neuroprotection

  • ZHANG Chao ,
  • CHEN Shenghui ,
  • HE Chengwei ,
  • WANG Yitao
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  • State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Seiences, University of Macau, Macau 999078, China

Received date: 2014-10-22

  Revised date: 2014-11-26

  Online published: 2015-03-03

Abstract

Hormesis refers to a dose-response relationship that is generally characterized as a biphasic dose response, and it induces an adaptive beneficial effect on a cell or organism at low doses but inhibits this effect at high doses. Recently, the hormesis concept attracts increasingly more attention in the field of the neural research, indicating that improving cellular adaptive ability provides a new idea and method for the prevention and treatment of neurological diseases. A class of useful stressors could markedly increase the neuronal resistance to more drastic stresses, which is defined as neurohormesis. This paper reviews the progress in hormesis research, neuroprotective effects and mechanisms of low doses of chemicals, radiation and calories restriction through inducing neurohormesis.

Cite this article

ZHANG Chao , CHEN Shenghui , HE Chengwei , WANG Yitao . Hormesis and neuroprotection[J]. Science & Technology Review, 2015 , 33(3) : 110 -113 . DOI: 10.3981/j.issn.1000-7857.2015.03.019

References

[1] Calabrese E J, Baldwin L A. Chemical hormesis: Its historical foundations as a biological hypothesis[J]. Human & Experimental Toxicology, 2000, 19(1): 2-31.
[2] DossM.Lowdoseradiationadaptiveprotectiontocontrol neurodegenerative diseases[J]. Dose-Response, 2014, 1(1): 1-11.
[3] Calabrese E J, Iavicoli I, Calabrese V. Hormesis: Why it is important to biogerontologists[J]. Biogerontology, 2012, 13(3): 215-235.
[4] Sielken R L, Stevenson D E. Some implications for quantitative risk assessment if hormesis exists[J]. Human & Experimental Toxicology, 1998, 17(5): 259-262.
[5] Wiegant F A C, Prins H A B, Van Wijk R. Postconditioning hormesis put in perspective: An overview of experimental and clinical studies[J]. Dose-Response, 2011, 9(2): 209-224.
[6] Guo L, Zhang X, Yang G, et al. Hormesis and its application in medicinal plant growing[J]. China Journal of Chinese Materia Medica, 2011, 36 (5): 525-529.
[7] Belz R G, Duke S O. Herbicides and plant hormesis[J]. Pest Management Science, 2014, 70(5): 698-707.
[8] Rithidech K N, Scott B R. Evidence for radiation hormesis after in vitro exposure of human lymphocytes to low doses of ionizing radiation[J]. Dose-Response, 2008, 6(3): 252-271.
[9] Vaiserman A M. Radiation hormesis: Historical perspective and implications for low-dose cancer risk assessment[J]. Dose-Response, 2010, 8(2): 172-191.
[10] Borak J, Sirianni G. Hormesis: Implications for cancer risk assessment [J]. Dose-Response, 2005, 3(3): 443-451.
[11] Sagan L A. On radiation, paradigms, and hormesis[J]. Science, 1989, 245(4918): 574, 621.
[12] Pandey K B, Rizvi S I. Anti-oxidative action of resveratrol: Implications for human health[J]. Arabian Journal of Chemistry, 2011, 4(3): 293-298.
[13] Calabrese E J, Mattson M P, Calabrese V. Resveratrol commonly displays hormesis: Occurrence and biomedical significance[J]. Human & Experimental Toxicology, 2010, 29(12): 980-1015.
[14] Vichi P, Tritton T R. Stimulation of growth in human and murine cells by adriamycin[J]. Cancer Research, 1989, 49(10): 2679-2682.
[15] Mattson M P, Cheng A. Neurohormetic phytochemicals: Low-dose toxins that induce adaptive neuronal stress responses[J]. Trends in Neurosciences, 2006, 29(11): 632-639.
[16] Mao L, Franke J. Hormesis in aging and neurodegeneration—A prodigy awaiting dissection[J]. International Journal of Molecular Sciences, 2013, 14(7): 13109-13128.
[17] Kroemer G, Mariño G, Levine B. Autophagy and the integrated stress response[J]. Molecular Cell, 2010, 40(2): 280-293.
[18] Kozlowski L, Garvis S, Bedet C, et al. The Caenorhabditis elegans HP1 family protein HPL-2 maintains ER homeostasis through the UPR and hormesis[J]. Proceedings of the National Academy of Sciences, 2014, 111(16): 5956-5961.
[19] Chen C Y, Jang J H, Li M H, et al. Resveratrol upregulates heme oxygenase-1 expression via activation of NF-E2-related factor 2 in PC12 cells[J]. Biochemical and Biophysical Research Communications, 2005, 331(4): 993-1000.
[20] Balogun E, Hoque M, Gong P, et al. Curcumin activates the haem oxygenase-1 gene via regulation of Nrf2 and the antioxidantresponsive element[J]. Biochemical Journal, 2003, 371: 887-895.
[21] Umemura K, Itoh T, Hamada N, et al. Preconditioning by sesquiterpene lactone enhances H2O2-induced Nrf2/ARE activation [J]. Biochemical and Biophysical Research Communications, 2008, 368 (4): 948-954.
[22] van der Veer E, Nong Z, O'Neil C, et al. Pre-B-Cell Colony-Enhancing Factor regulates NAD +-dependent protein deacetylase activity and promotes vascular smooth muscle cell maturation[J]. Circulation Research, 2005, 97(1): 25-34.
[23] Wang L M, Wang Y J, Cui M, et al. A dietary polyphenol resveratrol acts to provide neuroprotection in recurrent stroke models by regulating AMPK and SIRT1 signaling, thereby reducing energy requirements during ischemia[J]. European Journal of Neuroscience, 2013, 37(10): 1669-1681.
[24] Lipinski M M, Zheng B, Lu T, et al. Genome-wide analysis reveals mechanisms modulating autophagy in normal brain aging and in Alzheimer's disease[J]. Proceedings of the National Academy of Sciences, 2010, 107(32): 14164-14169.
[25] Matus S, Castillo K, Hetz C, et al. Hormesis: Protecting neurons against cellular stress in Parkinson disease[J]. Autophagy, 2012, 8(6): 997-1001.
[26] Chirumbolo S. The role of quercetin, flavonols and flavones in modulating inflammatory cell function[J]. Inflammation & Allergy-Drug Targets, 2010, 9(4): 263-285.
[27] Mattson M P, Meffert M K. Roles for NF-κB in nerve cell survival, plasticity, and disease[J]. Cell Death & Differentiation, 2006, 13(5): 852-860.
[28] Raja W K, Satti J, Liu G, et al. Dose response of MTLn3 cells to serial dilutions of arsenic trioxide and ionizing radiation[J]. Dose-Response, 2013, 11(1): 29-40.
[29] Selkoe D J. Alzheimer disease: Mechanistic understanding predicts novel therapies[J]. Annals of Internal Medicine, 2004, 140(8): 627-638.
[30] Morley J E, Farr S A. Hormesis and amyloid-β Protein: physiology or pathology?[J]. Journal of Alzheimer's Disease, 2012, 29(3): 487-492.
[31] Otani A, Kojima H, Guo C, et al. Low-dose-rate, low-dose irradiation delays neurodegeneration in a model of retinitis pigmentosa[J]. The American Journal of Pathology, 2012, 180(1): 328-336.
[32] Pollycove M, Feinendegen L E. Radiation-induced versus endogenous DNA damage: Possible effect of inducible protective responses in mitigating endogenous damage[J]. Human & Experimental Toxicology, 2003, 22(6): 290-306.
[33] Yang J L, Sykora P, Wilson III D M, et al. The excitatory neurotransmitter glutamate stimulates DNA repair to increase neuronal resiliency[J]. Mechanisms of Ageing and Development, 2011, 132(8): 405-411.
[34] Liao A C, Craver B M, Tseng B P, et al. Mitochondrial-targeted human catalase affords neuroprotection from proton irradiation[J]. Radiation Research, 2013, 180(1): 1-6.
[35] Schroeder J E, Richardson J C, Virley D J. Dietary manipulation and caloric restriction in the development of mouse models relevant to neurological diseases[J]. Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease, 2010, 1802(10): 840-846.
[36] Ludovico P, Burhans W C. Reactive oxygen species, ageing and the hormesis police[J]. FEMS Yeast Research, 2014, 14(1): 33-39.
[37] Kenyon C J. The genetics of ageing[J]. Nature, 2010, 464(7288): 504-512.
[38] MattsonMP.EnergyIntake,mealfrequency,andHealth:Aneurobiological perspective[J] Annual Review of Nutrition, 2005, 25: 237-260.
[39] Baker J, Meisner B A, Logan A J, et al. Physical activity and successful aging in Canadian older adults[J]. Journal of Aging and Physical Activity, 2009, 17(2): 223-235.
[40] Penedo F J, Dahn J R. Exercise and well-being: A review of mental and physical health benefits associated with physical activity[J]. Current Opinion in Psychiatry, 2005, 18(2): 189-193.
[41] Meeusen R. Exercise, nutrition & the brain[J]. Sports Science, 2013, 26(112): 1-6.
[42] Draganski B, Gaser C, Busch V, et al. Neuroplasticity: Changes in grey matter induced by training -Newly honed juggling skills show up as a transient feature on a brain-imaging scan[J]. Nature, 2004, 427 (6972): 311-312.
[43] Dirnagl U, Meisel A. Endogenous neuroprotection: Mitochondria as gateways to cerebral preconditioning[J]. Neuropharmacology, 2008, 55 (3): 334-344.
[44] Kitagawa K, Matsumoto M, Tagaya M, et al, Ischemic tolerance phenomenon found in the brain[J]. Brain Research, 1990, 1(528): 21-24.
[45] Hanley P J, Daut J. K-ATP channels and preconditioning: A reexamination of the role of mitochondrial KATp channels and an overview of alternative mechanisms[J]. Journal of Molecular and Cellular Cardiology, 2005, 1(39): 17-50.
[46] Abete P, Cacciatore F, Testa G, et al. Clinical application of ischemic preconditioning in the elderly[J]. Dose-Response, 2010, 1(8): 34-40.
[47] Ugidos A, Nystrom T, Caballero A, et al. Perspectives on the mitochondrial etiology of replicative aging in yeast[J]. Experimental Gerontology, 2010, 7-8(45): 512-515.
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