Effect of scutellarin on nitric oxide production in early stages of neuron damage induced by hydrogen peroxide
Effect of scutellarin on nitric oxide production in early stages of neuron damage induced by hydrogen peroxide
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DOI：
10.1016/j.phrs.2004.09.001
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发表时间：
2005-03-01
影响因子：
9.3
通讯作者：
Xu, HB
中科院分区：
文献类型：
--
作者：
Liu, H;Yang, XL;Xu, HB
本研究的目的是探讨灯盏乙素对过氧化氢诱导的神经元损伤早期阶段一氧化氮（NO）产生以及组成型一氧化氮合酶（cNOS）和诱导型一氧化氮合酶（iNOS）活性的调节功能。使用电化学传感器对活体大鼠神经元细胞的原代培养物进行 NO 产生的直接检测。过氧化氢显着增加了培养上清液中NO的水平，限定区域(500-6500s x pA)的总积分值达到3.68 x 10(6)。灯盏花乙素预处理导致总积分值以剂量依赖性方式下降（10、50和100 uM灯盏花乙素组分别为3.24 x 10(6)、2.15 x 10(6)、1.84 x 10(6)）。暴露于 2.0 mM 过氧化氢 2 小时后，脂质过氧化标志物丙二醛 (MDA) 水平显着升高。灯盏乙素可以抑制升高。过氧化氢还导致神经元活力显着丧失。与对照组相比，灯盏乙素显着减轻了损失。结果还表明，过氧化氢会增加 cNOS 的活性，而灯盏花乙素则显着抑制 cNOS 的活性。然而，神经元细胞暴露于过氧化氢并不会导致 iNOS 活性增加。总之，我们的结果表明，在过氧化氢诱导的神经元损伤的早期阶段，NO 的产生增加，灯盏乙素可以有效抑制它。此外，我们的结果表明 NO 产生的增加是由 cNOS 介导的。 (C) 2004 Elsevier Ltd. 保留所有权利。
The aims of the present study were to investigate the regulatory function of scutellarin on production of nitric oxide (NO) as well as activities of constitutive NO synthase (cNOS) and inducible NO synthase (iNOS) in early stages of neuron damage induced by hydrogen peroxide. Direct detection of NO production was performed on primary cultures of living rat neuronal cells with an electrochemical sensor. Hydrogen peroxide significantly increased culture supernatant levels of NO, the total integral value of the defined areas (500-6500s x pA) reached 3.68 x 10(6). Pre-treatment with scutellarin, caused the total integral value to decrease in a dose-dependent fashion (3.24 x 10(6), 2.15 x 10(6), 1.84 x 10(6) for groups 10, 50, and 100 uM scutellarin, respectively). After exposure to 2.0 mM hydrogen peroxide for 2h, malondialdehyde (MDA) level, a marker of lipid peroxidation, was remarkably increased. The elevation can be suppressed by scutellarin. Hydrogen peroxide also caused significant loss of neuron viability. In comparison with the control group, scutellarin significant attenuated the loss. Results also showed that hydrogen peroxide increased activity of cNOS, which was markedly inhibited by scutellarin. However, exposure of neuronal cells to hydrogen peroxide did not lead to an increase in iNOS activity. In conclusion, our results suggest that NO production, which increased in early stages of neuron damage induced by hydrogen peroxide can be effectively inhibited by scutellarin. Moreover, our results indicate that increase in NO production is mediated by cNOS. (C) 2004 Elsevier Ltd. All rights reserved.