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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >Effects of Apigenin on Glutamate-induced [Ca2+]i Increases in Cultured Rat Hippocampal Neurons
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Effects of Apigenin on Glutamate-induced [Ca2+]i Increases in Cultured Rat Hippocampal Neurons

机译：芹菜素对谷氨酸诱导的大鼠海马神经元[Ca2 +] i增加的影响

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摘要

Flavonoids have been shown to affect calcium signaling in neurons. However, there are no reports on the effect of apigenin on glutamate-induced calcium signaling in neurons. We investigated whether apigenin affects glutamate-induced increase of free intracellular Ca2+ concentration ([Ca2+]i) in cultured rat hippocampal neurons, using fura-2-based digital calcium imaging and microfluorimetry. The hippocampal neurons were used between 10 and 13 days in culture from embryonic day 18 rats. Pretreatment of the cells with apigenin (1 μM to 100 μM) for 5 min inhibited glutamate (100 μM, 1 min) induced [Ca2+]i increase, concentration-dependently. Pretreatment with apigenin (30 μM) for 5 min significantly decreased the [Ca2+]i responses induced by two ionotropic glutamate receptor agonists, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic (AMPA, 10 μM, 1 min) and N-methyl-D-aspartate (NMDA, 100 μM, 1 min), and significantly inhibited the AMPA-induced peak currents. Treatment with apigenin also significantly inhibited the [Ca2+]i response induced by 50 mM KCl solution, decreased the [Ca2+]i responses induced by the metabotropic glutamate receptor agonist, (S)-3,5-dihydroxyphenylglycine (DHPG, 100 μM, 90 s), and inhibited the caffeine (10 mM, 2 min)-induced [Ca2+]i responses. Furthermore, treatment with apigenin (30 μM) significantly inhibited the amplitude and frequency of 0.1 mM [Mg2+]o-induced [Ca2+]i spikes. These data together suggest that apigenin inhibits glutamate-induced calcium signaling in cultured rat hippocampal neurons.
机译：黄酮类化合物已显示会影响神经元中的钙信号传导。但是，没有关于芹菜素对谷氨酸诱导的神经元钙信号传导作用的报道。我们调查芹菜素是否影响谷氨酸诱导的大鼠海马神经元细胞内游离Ca 2 + 浓度（[Ca 2 + ] i ）的增加，使用基于fura-2的数字钙成像和微荧光法。在培养第18天胚胎的大鼠中，在培养的10到13天之间使用海马神经元。用芹菜素（1μM至100μM）预处理细胞5分钟，抑制了谷氨酸（100μM，1分钟）诱导的[Ca 2 + ] i 升高，浓度为-依附芹菜素（30μM）预处理5分钟可显着降低由两种离子型谷氨酸受体激动剂α-氨基-3-羟基-苯丙氨酸诱导的[Ca 2 + ] i 反应5-甲基-4-异恶唑丙酸（AMPA，10μM，1分钟）和N-甲基-D-天冬氨酸（NMDA，100μM，1分钟），并显着抑制了AMPA诱导的峰值电流。芹菜素处理还显着抑制了50 mM KCl溶液诱导的[Ca 2 + ] i 反应，降低了[Ca 2 + ] <代谢型谷氨酸受体激动剂（S）-3,5-二羟基苯基甘氨酸（DHPG，100μM，90 s）诱导的sub> i 反应，并抑制咖啡因（10 mM，2分钟）诱导的[Ca 2 + ] i 响应。此外，芹菜素（30μM）处理显着抑制了0.1 mM [Mg 2 + ] o 诱导的[Ca 2 + ] i 峰值。这些数据一起表明芹菜素在培养的大鼠海马神经元中抑制谷氨酸诱导的钙信号传导。

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