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尼麦角林对大鼠神经细胞系过氧化氢毒性的保护作用。

Protective effects of nicergoline against hydrogen peroxide toxicity in rat neuronal cell line.

作者信息

Iwata E, Miyazaki I, Asanuma M, Iida A, Ogawa N

机构信息

Department of Neuroscience, Institute of Molecular and Cellular Medicine, Okayama University Medical School, Japan.

出版信息

Neurosci Lett. 1998 Jul 17;251(1):49-52. doi: 10.1016/s0304-3940(98)00489-3.

Abstract

We examined the effects of nicergoline on hydrogen peroxide (H2O2)-induced neurotoxicity in cultured rat neuronal cell line (B50). H2O2 induced death of B50 cells in a dose-dependent manner. The H2O2-induced neuronal cell death was significantly decreased in B50 cells maintained in the presence of nicergoline. We compared the levels of antioxidants (glutathione, catalase and superoxide dismutase) in nicergoline-treated and untreated B50 cells. Lipid peroxidation products (thiobarbituric acid reactive substances, TBARS) levels were also measured. Cultures treated with nicergoline had higher levels of catalase activity. TBARS level was significantly lower in nicergoline-treated cells than in untreated cells. Our results suggest that nicergoline may induce the up-regulation of intracellular antioxidant defences and protect the neuronal cells against oxidative stress.

摘要

我们研究了尼麦角林对过氧化氢(H2O2)诱导的大鼠神经元细胞系(B50)神经毒性的影响。H2O2以剂量依赖性方式诱导B50细胞死亡。在存在尼麦角林的情况下培养的B50细胞中,H2O2诱导的神经元细胞死亡显著减少。我们比较了尼麦角林处理组和未处理组B50细胞中抗氧化剂(谷胱甘肽、过氧化氢酶和超氧化物歧化酶)的水平。还测量了脂质过氧化产物(硫代巴比妥酸反应性物质,TBARS)水平。用尼麦角林处理的培养物具有较高的过氧化氢酶活性水平。尼麦角林处理组细胞中的TBARS水平显著低于未处理组细胞。我们的结果表明,尼麦角林可能诱导细胞内抗氧化防御上调,并保护神经元细胞免受氧化应激。

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