参考文献/References:
[1] Du Y, Chen CP, Tseng CY, et al. Astroglia-mediated effects
of uric acid to protect spinal cord neurons from glutamate
toxicity [J]. Glia, 2007, 55(5): 463-472.
[2] Nakamichi N, Kambe Y, Oikawa H, et al. Protection by exo-
genous pyruvate through a mechanism related to monocar-
boxylate transporters against cell death induced by hydrogen
peroxide in cultured rat cortical neurons [J]. J Neurochem,
2005, 93(1): 84-93.
[3] Wang XF, Cynader MS. Pyruvate released by astrocytes pro-
tects neurons from copper-catalyzed cysteine neurotoxicity
[J]. J Neurosci, 2001, 21(10): 3322-3331.
[4] Lobner D, Canzoniero LM, Manzerra P, et al. Zinc-induced
neuronal death in cortical neurons [J]. Cell Mol Biol (Noisy-
legrand), 2000, 46(4):797-806.
[5] Lee JY, Kim YH, Koh JY. Protection by pyruvate against
transient forebrain ischemia in rats [J]. J Neurosci, 2001, 21
(20): RC171.
[6] Suh SW, Aoyama K, Matsumori Y, et al. Pyruvate adminis-
tered after severe hypoglycemia reduces neuronal death and
cognitive impairment [J]. Diabetes, 2005, 54(5): 1452-1458.
[7] Yi JS, Kim TY, Kyu Kim D, et al. Systemic pyruvate admi-
nistration markedly reduces infarcts and motor deficits in rat
models of transient and permanent focal cerebral ischemia
[J]. Neurobiol Dis, 2007, 26(1): 94-104.
[8] 包娜然,卯新民. 血清乳酸、丙酮酸、琥珀酸的气相色谱测
定[J]. 兰州医学院学报,1991, 17(2):72-74.
[9] Kitagawa K, Matsumoto M, Tagaya M, et al. 'Ischemic
tolerance' phenomenon found in the brain [J]. Brain Res,
1990,528(1): 21-24.
[10] Bond A, Lodge D, Hicks CA, et al. NMDA receptor antago-
nism, but not AMPA receptor antagonism attenuates indu-
ced ischaemic tolerance in the gerbil hippocampus [J]. Eur
J Pharmacol, 1999, 380(2-3): 91-99.
[11] Perez-Pinzon MA. Mechanisms of neuroprotection during
ischemic preconditioning: lessons from anoxic tolerance
[J]. Comp Biochem Physiol A Mol Integr Physiol, 2007, 147
(2): 291-299.
[12] Liu Y, Xiong L, Chen S, et al. Isoflurane tolerance against
focal cerebral ischemia is attenuated by adenosine A1 re-
ceptor antagonists[J]. Can J Anaesth, 2006, 53(2): 194-201.
[13] Zhao P, Huang Y, Zuo Z. Opioid preconditioning induces
opioid receptor-dependent delayed neuroprotection against
ischemia in rats [J]. J Neuropathol Exp Neurol, 2006, 65
(10): 945-952.
[14] Mehta SL, Manhas N, Raghubir R. Molecular targets in ce-
rebral ischemia for developing novel therapeutics [J]. Brain
Res Rev, 2007, 54(1): 34-66.
[15] Yin XH, Zhang QG, Miao B, et al. Neuroprotective effects of
preconditioning ischaemia on ischaemic brain injury
through inhibition of mixed-lineage kinase 3 via NMDA
receptor-mediated Akt1 activation [J]. J Neurochem, 2005,
93(4): 1021-1029.
[16] Miao B, Yin XH, Pei DS, et al. Neuroprotective effects of
preconditioning ischemia on ischemic brain injury through
down-regulating activation of JNK1/2 via N-methyl-D-
aspartate receptor-mediated Akt1 activation [J]. J Biol
Chem, 2005, 280(23): 21693-21699.
[17] Walton M, Sirimanne E, Williams C, et al. The role of the
cyclic AMP-responsive element binding protein (CREB) in
hypoxic-ischemic brain damage and repair [J]. Brain Res
Mol Brain Res, 1996, 43(1-2): 21-29.
[18] Bergeron M, Gidday JM, Yu AY, et al. Role of hypoxia-in-
ducible factor-1 in hypoxia-induced ischemic tolerance in
neonatal rat brain [J]. Ann Neurol, 2000, 48(3): 285-296.
[19] Ohtsuki T, Ruetzler CA, Tasaki K, et al. Interleukin-1 me-
diates induction of tolerance to global ischemia in gerbil hi-
ppocampal CA1 neurons [J]. J Cereb Blood Flow Metab,
1996, 16(6): 1137-1142.
[20] Nawashiro H, Tasaki K, Ruetzler CA, et al. TNF-alpha pre-
treatment induces protective effects against focal cerebral
ischemia in mice [J]. J Cereb Blood Flow Metab, 1997, 17
(5): 483-490.
[21] Mattson MP, Goodman Y, Luo H, et al. Activation of NF-
kappaB protects hippocampal neurons against oxidative
stress-induced apoptosis: evidence for induction of manga-
nese superoxide dismutase and suppression of peroxynitrite
production and protein tyrosine nitration [J]. J Neurosci Res,
1997, 49(6): 681-697.
[22] Sheline CT, Behrens MM, Choi DW. Zinc-induced cortical
neuronal death: contribution of energy failure attributable to
loss of NAD(+) and inhibition of glycolysis [J]. J Neurosci,
2000, 20(9): 3139-3146.