[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.