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首页> 外文期刊>Journal of pharmacological sciences. >Protective effect of zinc against ischemic neuronal injury in a middle cerebral artery occlusion model.
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Protective effect of zinc against ischemic neuronal injury in a middle cerebral artery occlusion model.

机译:锌对大脑中动脉闭塞模型中缺血性神经元损伤的保护作用。

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In this study, we investigated the effect of vesicular zinc on ischemic neuronal injury. In cultured neurons, addition of a low concentration (under 100 microM) of zinc inhibited both glutamate-induced calcium influx and neuronal death. In contrast, a higher concentration (over 150 microM) of zinc decreased neuronal viability, although calcium influx was inhibited. These results indicate that zinc exhibits biphasic effects depending on its concentration. Furthermore, in cultured neurons, co-addition of glutamate and CaEDTA, which binds extra-cellular zinc, increased glutamate-induced calcium influx and aggravated the neurotoxicity of glutamate. In a rat transient middle cerebral artery occlusion (MCAO) model, the infarction volume, which is related to the neurotoxicity of glutamate, increased rapidly on the intracerebral ventricular injection of CaEDTA 30 min prior to occlusion. These results suggest that zinc released from synaptic vesicles may provide a protective effect against ischemic neuronal injury.
机译:在这项研究中,我们调查了水泡锌对缺血性神经元损伤的影响。在培养的神经元中,添加低浓度(低于100 microM)的锌会抑制谷氨酸诱导的钙内流和神经元死亡。相反,较高的锌浓度(超过150 microM)会降低神经元活力,尽管会抑制钙内流。这些结果表明锌根据其浓度表现出两相效应。此外,在培养的神经元中,谷氨酸和CaEDTA的共添加会结合细胞外锌,增加谷氨酸诱导的钙内流,并加剧谷氨酸的神经毒性。在大鼠短暂性大脑中动脉闭塞(MCAO)模型中,与谷氨酸的神经毒性有关的梗死体积在闭塞前30分钟经脑室内注射CaEDTA迅速增加。这些结果表明,从突触小泡释放的锌可能提供针对缺血性神经元损伤的保护作用。

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