Neuronal NOS inhibitor that reduces oxidative DNA lesions and neuronal sensitivity increases the expression of intact c-fos transcripts after brain injury.
Neuronal NOS inhibitor that reduces oxidative DNA lesions and neuronal sensitivity increases the expression of intact c-fos transcripts after brain injury.
复制标题
神经元 NOS 抑制剂可减少氧化 DNA 损伤和神经元敏感性，增加脑损伤后完整 c-fos 转录物的表达。
DOI：
10.1007/bf02258375
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发表时间：
2001
影响因子：
11
通讯作者：
Liu,PK
中科院分区：
文献类型：
--
作者：
Cui,J;Liu,PK
在氧化应激的反应中，缺血脑在其核基因含有基因损伤时诱导立即早期基因。减少基因损伤的抗氧化剂也减少了细胞死亡。为了研究神经元敏感性的机制，我们采用Long-Evans hooded大鼠局灶性脑缺血-再灌注模型，研究了缺血-再灌注型脑损伤后c-fosgene的转录。我们观察到脑损伤后即刻缺血皮质c-fos mRNA显著增加（P < 0.01）。然而，c-fos的转录是敏感的RNA酶A保护试验（RPA）在再灌注。当3-溴-7-硝基吲哚（25 mg/kg，腹腔注射）、已知消除一氧化氮，基因损伤和神经元敏感性。我们的数据表明，神经元型一氧化氮合酶和氧化损伤基因的异常mRNA可能与神经元的敏感性有关。
In response to oxidative stress, the ischemic brain induces immediate early genes when its nuclear genes contain gene damage. Antioxidant that reduces gene damage also reduces cell death. To study the mechanism of neuronal sensitivity, we investigated the transcription of the c-fosgene after brain injury of the ischemia-reperfusion type using focal cerebral ischemia-reperfusion in Long-Evans hooded rats. We observed a significant (p < 0.01) increase in c-fos mRNA in the ischemic cortex immediately after brain injury. However, the c-fos transcript was sensitive to RNase A protection assay (RPA) upon reperfusion. The transcript became significantly resistant to RPA (42%, p < 0.03) when 3-bromo-7-nitroindazole (25 mg/kg, i.p.), known to abolish nitric oxide, gene damage and neuronal sensitivity, was injected. Our data suggest that neuronal nitric oxide synthase and aberrant mRNA from genes with oxidative damage could be associated with neuronal sensitivity.