B7263
N-叔丁基-α-苯基硝酮
≥98% (GC)
别名:
N-苯亚甲基-叔丁胺-N-氧化物, PBN, 苯基·N-叔丁基硝酮
质量水平
方案
≥98% (GC)
表单
powder
颜色
white
mp
73-74 °C (lit.)
溶解性
DMSO: soluble
储存温度
−20°C
SMILES字符串
CC(C)(C)[N+](\[O-])=C\c1ccccc1
InChI
1S/C11H15NO/c1-11(2,3)12(13)9-10-7-5-4-6-8-10/h4-9H,1-3H3/b12-9-
InChI key
IYSYLWYGCWTJSG-XFXZXTDPSA-N
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应用
N-叔丁基-α-苯基硝酮已用于：
- 用作Dneasy Blood&血液组织缓冲液组分，以保留从人类非致瘤性上皮性乳腺癌（MCF10A）细胞中提取的氧化态DNA
- 用作微胶质（MG）细胞系活性氧(ROS)自由基清除试剂
- 衰减不稳定口腔鳞状细胞癌（GU-OSCC）中的成纤维细胞衰老
生化/生理作用
N-叔丁基-α-苯基硝酮（PBN）是一种常用的自由基自旋捕获剂。
N-叔丁基-α-苯基硝酮（PBN）是一种常用的自由基自旋捕获剂。已有研究表明，PBN具有自由基清除活性以及抑制环氧合酶-2活性的能力，因此，它可以减少兔皮质中栓子诱导的脑微梗死的数量并预防肿瘤形成。据报道，PBN可抑制诱导型一氧化氮合酶（iNOS），从而防止一氧化氮（NO）过量产生。 PBN以100 mg/kg腹腔注射，可减少氟替尔诱导大鼠癫痫持续状态中的黑质网状部坏死。它可以预防癫痫动物模型中某些类型的创伤后致癫痫事件。已有研究发现，大鼠的PBN致死剂量约为100 mg/100 g体重（0.564 mmol/100Å g）。
储存分类代码
11 - Combustible Solids
WGK
WGK 3
闪点(°F)
Not applicable
闪点(°C)
Not applicable
个人防护装备
Eyeshields, Gloves, type N95 (US)
Progression of genotype-specific oral cancer leads to senescence of cancer-associated fibroblasts and is mediated by oxidative stress and TGF-beta
Hassona Y, et al.
Carcinogenesis, 34(6), 1286-1295 (2013)
Genome-wide mapping of 8-oxo-7, 8-dihydro-2?-deoxyguanosine reveals accumulation of oxidatively-generated damage at DNA replication origins within transcribed long genes of mammalian cells
Amente S, et al.
Nucleic Acids Research, 47(1), 221-236 (2018)
microRNA-34a-mediated down-regulation of the microglial-enriched triggering receptor and phagocytosis-sensor TREM2 in age-related macular degeneration
Bhattacharjee S, et al.
Testing, 11(3), e0150211-e0150211 (2016)
D A Butterfield et al.
Annals of the New York Academy of Sciences, 854, 448-462 (1999-02-03)
The free radical theory of aging proposes that reactive oxygen species (ROS) cause oxidative damage over the lifetime of the subject. It is the cumulative and potentially increasing amount of accumulated damage that accounts for the dysfunctions and pathologies seen
June Yowtak et al.
Pain, 152(4), 844-852 (2011-02-08)
Although both a loss of spinal inhibitory neurotransmission and the involvement of oxidative stress have been regarded as important mechanisms in the pathogenesis of pain, the relationship between these 2 mechanisms has not been studied. To determine whether reactive oxygen
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