Molecular hydrogen in drinking water Protects against neurodegenerative changes induced by traumatic brain injury

PLoS ONE

Volumn 9, Issue 9, 2014, Pages

  Dohi, Kenji ^a,b   Kraemer, Brian C ^a,c   Erickson, Michelle A ^a   McMillan, Pamela J ^a,c   Kovac, Andrej ^a,c   Flachbartova, Zuzana ^d   Hansen, Kim M ^a,c   Shah, Gul N ^e   Sheibani, Nader ^f   Salameh, Therese ^a,c   Banks, William A ^a,c  

^a VA PUGET SOUND HEALTH CARE SYSTEM   (United States)

^b JIKEI UNIVERSITY SCHOOL OF MEDICINE   (Japan)

^c UNIVERSITY OF WASHINGTON SCHOOL OF MEDICINE   (United States)

^d UNIVERSITY OF VETERINARY MEDICINE   (Slovakia)

^e SAINT LOUIS UNIVERSITY SCHOOL OF MEDICINE   (United States)

^f UNIVERSITY OF WISCONSIN SCHOOL OF MEDICINE AND PUBLIC HEALTH   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ADENOSINE TRIPHOSPHATE; AMYLOID BETA PROTEIN; AMYLOID PRECURSOR PROTEIN; AQUAPORIN 4; CARBOHYDRATE; CYCLOPHILIN A; CYTOKINE; DRINKING WATER; GELATINASE A; GELATINASE B; HYDROGEN; HYPOXIA INDUCIBLE FACTOR 1ALPHA; NUCLEOTIDE; TAU PROTEIN; ANTIOXIDANT; NEUROPROTECTIVE AGENT;

ALZHEIMER DISEASE; ANIMAL EXPERIMENT; ANIMAL TISSUE; ARTICLE; BRAIN EDEMA; BRAIN HOMOGENATE; CARBOHYDRATE METABOLISM; CELL MIGRATION; CONTROLLED STUDY; CYTOKINE RELEASE; DEGENERATIVE DISEASE; EDEMA; GENE EXPRESSION; IMMUNOHISTOCHEMISTRY; LEUKOCYTE MIGRATION; MALE; MOUSE; NERVOUS SYSTEM INFLAMMATION; NONHUMAN; NUCLEOTIDE BINDING SITE; OXIDATIVE STRESS; PARKINSON DISEASE; PROTEIN EXPRESSION; RISK FACTOR; TRAUMATIC BRAIN INJURY; ANIMAL; BLOOD; BRAIN; BRAIN INJURIES; C57BL MOUSE; COMPLICATION; DRUG EFFECTS; GENE EXPRESSION REGULATION; METABOLISM; PATHOLOGY;

ANIMALS; ANTIOXIDANTS; BRAIN; BRAIN EDEMA; BRAIN INJURIES; CYTOKINES; DRINKING WATER; GENE EXPRESSION REGULATION; HYDROGEN; MALE; MICE, INBRED C57BL; NEUROPROTECTIVE AGENTS;

EID: 84907476719     PISSN: None     EISSN: 19326203     Source Type: Journal    
DOI: 10.1371/journal.pone.0108034     Document Type: Article

References (34)

1. Sayer NA (2012) Traumatic brain injury and its neuropsychiatric sequelae in war veterans. Annu Rev Med 63: 405-419.
2. Wick JY (2012) Traumatic brain injury: special problem, special care. Consult Pharm 27: 392-399.
3. Cernak I (2005) Animal models of head trauma. NeruoRx 2: 410-422.
4. Bazarian JJ, Cernak I, Noble-Haeusslein L, Potolicchio S, Temkin N (2009) Long-term neurologic outcomes after traumatic brain injury. J Head Trauma Rehabil 24: 439-451.
5. Deng Y, Thompson BM, GAo X, Hall ED (2007) Temporal relationship of peroxynitrite-induced oxidative damage, calpain-mediated cytoskeletal degradation and neurodegeneration after traumatic brain injury. Experimental Neurology 205: 154-165.
6. Hawkins BE, Krishnamurthy S, Castillo-Carranza DL, Sengupta U, Prough DS, et al. (2013) Rapid Accumulation of Endogenous Tau Oligomers in a Rat Model of Traumatic Brain Injury: Possible Link Between TBI and Sporadic Tauopathies. J Biol Chem.
7. Johnson VE, Stewart W, Smith DH (2012) Widespread tau and amyloid-beta pathology many years after a single traumatic brain injury in humans. Brain Pathol 22: 142-149.
8. Morganti-Kossman MC, Lenzlinger PM, Hans V, Stahel P, Csuka E, et al. (1997) Production of cytokines following brain injury: beneficial and deleterious for the damaged tissue. Molecular Psychiatry 2: 133-136.
9. Ohsawa I, Ishikawa M, Takahashi K, Watanabe M, Nishimaki K, et al. (2007) Hydrogen acts as a therapeutic antioxidant by selectively reducing cytotoxic oxygen radicals. Nature Medicine 13: 688-694.
10. Miyamoto K, Tsumuraya T, Ohtaki H, Dohi K, Satoh K, et al. (2014) PACAP38 suppresses cortical damage in mice with traumatic brain injury by enhancing antioxidant activity. J Mol Neurosci epub.
11. Keep RF, Hua Y, Xi G (2012) Brain water content. A misunderstood measurement? Transl Stroke Res 3: 263-265.
12. Ishihara T, Hong M, Zhang B, Nakagawa Y, Lee MK, et al. (1999) Age-dependent emergence and progression of a tauopathy in transgenic mice overexpressing the shortest human tau isoform. Neuron 24: 751-762.
13. Guthrie CR, Schellenberg GD, Kraemer BC (2009) SUT-2 potentiates tau-induced neurotoxicity in Caenorhabditis elegans. Hum Mol Genet 18: 1825-1838.
14. Erickson MA, Niehoff ML, Farr SA, Morley JE, Dillman LA, et al. (2012) Peripheral administration of antisense oligonucleotides targeting the amyloid beta protein precursor reverses ABPP and LRP-1 overexpression in aged SAMP8 mouse brain. J Alzheimer's Dis 28: 951-960.
15. Silverberg GD, Messier AA, Miller MC, Machan JT, Majmudar SS, et al. (2010) Amyloid efflux transporter expression at the blood-brain barrier declines in normal aging. J Neuropathol Exp Neurol 69: 1034-1043.
16. De Gasperi R, Gama Sosa MA, Kim SH, Steele JW, Shaughness MC, et al. (2012) Acute blast injury reduces brain abeta in two rodent species. Front Neurol 3: 177.
17. Banks WA, Fasold MB, Kastin AJ (1997) Measurement of efflux rate from brain to blood. In: Irvine GB, Williams CH, editors. Methods in Molecular Biology: Neuropeptides Protocols. Totowa, NJ: Humana Press. 353-360.
18. Shah GN, Price TO, Banks WA, Morofuji Y, Kovac A, et al. (2012) Pharmacological inhibition of mitochondrial carbonic anhydrases protects mouse cerebral pericytes from high glucose-induced oxidative stress and apoptosis. J Pharmacol Exp Therap 344: 637-645.
19. Higashida T, Kreipke CW, Rafols JA, Peng C, Schafer S, et al. (2011) The role of hypoxia-inducible factor-1alpha, aquaporin-4, and matrix metalloproteinase-9 in blood-brain barrier disruption and brain edema after traumatic brain injury. J Neurosurg 114: 92-101.
20. Bell RD, Winkler EA, Singh I, Sagare AP, Deane R, et al. (2012) Apolipoprotein E controls cerebrovascular integrity via cyclophilin A. Nature 485: 512-516.
21. Halliday MR, Pomara N, Sagare AP, Mack WJ, Frangione B, et al. (2013) Relationship between cyclophilin A levels and matrix metalloproteinase 9 activity in cerebrospinal fluid of cognitively normal apolipoprotein E4 carriers and blood-brain barrier breakdown. JAMA 70: 1198-1200.
22. Reyes TM, Fabry Z, Coe CL (1999) Brain endothelial cell production of a neuroprotective cytokine, interleukin-6, in response to noxious stimuli. Brain Research 851: 215-220.
23. Verma S, Nakaoke R, Dohgu S, Banks WA (2006) Release of cytokines by brain endothelial cells: a polarized response to lipopolysaccharide. Brain, Behavior, and Immunity 20: 449-455.
24. Kovac A, Erickson MA, Banks WA (2011) Brain microvascular pericytes are immunoactive in culture: cytokine, chemokine, nitric oxide, and LRP-1 expression in response to lipopolysaccharide. Journal of Neuroinflammation 8: 139.
25. Pan W, Banks WA, Kennedy MK, Gutierrez EG, Kastin AJ (1996) Differential permeability of the BBB in acute EAE: enhanced transport of TNF-alpha. American Journal of Physiology 271: E636-E642.
26. Pan W, Kastin AJ (2001) Increase in TNF alpha transport after SCI is specific for time, region, and type of lesion. Experimental Neurology 170: 357-363.
27. Pan W, Banks WA, Kastin AJ (1998) Permeability of the blood-brain barrier to neurotrophins. Brain Research 788: 87-94.
28. Pan W, Cain C, Yu Y, Kastin AJ (2006) Receptor-mediated transport of LIF across blood-spinal cord barrier is upregulated after spinal cord injury. Journal of Neuroimmunology 174: 119-125.
29. Jin X, Ishii H, Bai Z, Itokazu T, Yamashita T (2012) Temporal changes in cell marker expression and cellular infliltration in a controlled cortical impact model in adult male C57BL/6 mice. PLoS One 7: e41892.
30. Pan W, Zadina JE, Harlan RE, Weber JT, Banks WA, et al. (1997) Tumor necrosis factor-alpha: a neuromodulator in the CNS. Neuroscience and Biobehavioral Reviews 21: 603-613.
31. Price TO, Eranki V, Banks WA, Ercal N, Shah GN (2012) Topiramate treatment protects blood-brain barrier pericytes from hyperglycemia-induced oxidative damage in diabetic mice. Endocrinology 153: 362-372.
32. Shah GN, Price TO, Banks WA, Morofuji Y, Kovac A, et al. (2013) Pharmacological inhibition of mitochondrial carbonic anhydrases protects mouse cerebral pericytes from high glucose-induced oxidative stress and apoptosis. J Pharmacol Exp Therap 344: 637-645.
33. Jagendorf AT, Uribe E (1966) ATP formation caused by acid-base transition of spinach chloroplasts. Proc Natl Acad Sci USA 55: 170-177.
34. Soustiel JF, Larisch S (2010) Mitochondrial damage: a target for new therapeutic horizons. Neurotherapeutics 7: 13-21.