7-Nitroindazole reduces ischemia-induced increment of apoptosis and cell proliferation in the dentate gyrus of rats

M. Jang, M. Shin, Hyun-kyung Chang, Taeck-Hyun Lee, Hee-Hyuk Lee, Mal-Soon Shin, Chang-Ju Kim, J. Kang, Seon-Pyo Hong, Sonhae Cho
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引用次数: 2

Abstract

Nitric oxide is synthesized from L-arginine by nitric oxide synthase (NOS), and it is a free radical with signaling functions. Neuronal nitric oxide synthase (nNOS) is mainly expressed in the central nervous system, and it has been implicated in the pathogenesis of brain injury such as ischemia. In the present study, the effects of 7-nitroindazole, which specifically inhibits nNOS, on apoptosis and cell proliferation int he dentate gyrus after transient global ischemia in gerbils were investigated. Enhanced apoptotic neuronal cell death and cell proliferation were observed in the dentate gyrus of ischemic gerbils. However, 7-nitroindazole suppressed the ischemia-induced apoptosis and cell proliferation. These results suggest that 7-nitroindazole has an inhibitive effect on apoptosis and cell proliferation following transient global ischemia. The present study shows that nitric oxide, the synthesis of which is augmented by ischemia, plays an important role in the regulation of apoptosis and cell proliferation following ischemic injury.
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7-硝基吲唑降低缺血诱导的大鼠齿状回细胞凋亡和细胞增殖
一氧化氮是由l -精氨酸由一氧化氮合酶(NOS)合成的,是一种具有信号功能的自由基。神经元型一氧化氮合酶(Neuronal nitric oxide synthase, nNOS)主要表达于中枢神经系统,参与脑缺血等脑损伤的发病机制。本实验研究了特异性抑制nNOS的7-硝基茚唑对沙鼠短暂性全脑缺血后齿状回细胞凋亡和细胞增殖的影响。缺血沙鼠齿状回细胞凋亡和细胞增殖增强。而7-硝基吲唑对缺血诱导的细胞凋亡和细胞增殖有抑制作用。结果表明,7-硝基吲达唑对短暂性全脑缺血后的细胞凋亡和细胞增殖具有抑制作用。目前的研究表明,一氧化氮的合成在缺血损伤后的细胞凋亡和细胞增殖的调控中起重要作用。
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