N-叔丁基-α-(2-磺基苯基)硝酮钠盐
N-叔丁基-α-(2-磺基苯基)硝酮钠盐结构式
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常用名 | N-叔丁基-α-(2-磺基苯基)硝酮钠盐 | 英文名 | N-tert-Butyl-α-(2-sulfophenyl)nitrone sodium salt |
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| CAS号 | 73475-11-3 | 分子量 | 279.28800 | |
| 密度 | N/A | 沸点 | N/A | |
| 分子式 | C11H14NNaO4S | 熔点 | 246 °C (dec.) (lit.) | |
| MSDS | 中文版 美版 | 闪点 | N/A | |
| 符号 |
GHS07 |
信号词 | Warning |
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Atypical effect of some spin trapping agents: reversible inhibition of acetylcholinesterase.
Free Radic. Biol. Med. 28(4) , 597-603, (2000) N-tert-butyl-alpha-phenylnitrone (PBN), a widely used nitrone-based free radical trap was recently shown to prevent acetylcholinesterase (AChE) inhibitors induced muscle fasciculations and brain seizures while being ineffective against glutamergic or choliner... |
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Effects of cytisine on hydroxyl radicals in vitro and MPTP-induced dopamine depletion in vivo.
Eur. J. Pharmacol. 360(2-3) , 155-63, (1998) The potential new iron-chelator cytisine and the radical scavenger N-tert-butyl-alpha-(2-sulfophenyl) nitrone (S-PBN) were incubated in a Fenton system and hydroxyl radical formation was measured with the salicylate trapping assay. Both cytisine and S-PBN red... |
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Comparison of the radical trapping ability of PBN, S-PPBN and NXY-059.
Free Radic. Res. 34(4) , 417-26, (2001) The nitrones alpha-phenyl-N-tert-butyl nitrone (PBN), sodium 2-sulfophenyl-N-tert-butyl nitrone (S-PBN) and disodium 2,4-disulfophenyl-N-tert-butyl nitrone (NXY-059) are neuroprotective in a variety of rodent models. The objective of the current studies was t... |
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The free radical scavenger S-PBN significantly prolongs DSG-mediated graft survival in experimental xenotransplantation.
Xenotransplantation 19(3) , 166-76, (2012) Nitrones such as 2-sulfo-phenyl-N-tert-butyl nitrone (S-PBN) are known to trap and stabilize free radicals and to reduce inflammation. Recently, S-PBN was shown to reduce infiltration of T lymphocytes and the expression of adhesion molecules on the endotheliu... |
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Lipoic acid improves survival in transgenic mouse models of Huntington's disease.
Neuroreport 12(15) , 3371-3, (2001) There is substantial evidence implicating excitotoxicity and oxidative damage in the pathogenesis of Huntington's disease (HD). We therefore examined whether the antioxidants 2-sulpho-tert-phenyibutyinitrone (S-PBN) and alpha-lipoic acid could exert neuroprot... |
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Comparison of neuroprotective effects induced by alpha-phenyl-N-tert-butyl nitrone (PBN) and N-tert-butyl-alpha-(2 sulfophenyl) nitrone (S-PBN) in lithium-pilocarpine status epilepticus.
Neurotoxicology 26(6) , 969-79, (2005) The status epilepticus (SE) induced in rats by lithium-pilocarpine (Li-pilo) shares many common features with soman-induced SE including extensive limbic neuropathology. Reactive oxygen species are hypothesized to play a role in the SE induced neuropathology ... |
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Neonatal rat hypoxia-ischemia: Effect of the anti-oxidant mitoquinol, and S-PBN.
Pediatr. Int. 50(4) , 481-8, (2008) The production of oxygen free radicals after perinatal hypoxia-ischemia is thought to play a critical role in the pathogenesis of the brain injury. Administration of anti-oxidants may thus be neuroprotective. The aim of the present study was to investigate th... |
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Neurotrophin potentiation of iron-induced spinal cord injury.
Neuroscience 115(3) , 931-9, (2002) Previous studies have shown that pretreatment with neurotrophins can potentiate the vulnerability of cultured neurons to excitotoxic and free radical-induced necrosis, in contrast to their well known neuroprotective effects against apoptosis. Here we tested t... |
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Investigating the free radical trapping ability of NXY-059, S-PBN and PBN.
Free Radic. Res. 41(9) , 1047-52, (2007) The spin trapping ability of the nitrones 2,4-disulphophenyl-N-tert-butyl nitrone (NXY-059), 2-sulphophenyl-N-tert-butyl nitrone (S-PBN) and alpha-phenyl-N-tert-butyl nitrone (PBN) for both hydroxyl and methanol radicals was investigated using electron parama... |
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In vitro neuroprotection against oxidative stress by pre-treatment with a combination of dihydrolipoic acid and phenyl-butyl nitrones.
Neurotox. Res. 5(4) , 265-272, (2003) One consequence of trauma to the CNS is the production and liberation, from damaged tissue, of large amounts of oxygen-centered free radicals or reactive oxygen species (ROS). An excessive production of ROS can overwhelm the endogenous antioxidant defense sys... |