丹皮酚减轻大鼠海马神经元缺糖缺氧损伤及抑制NMDA受体激活

宋宁宁 武继彪 魏欣冰 管华诗 张岫美

丹皮酚减轻大鼠海马神经元缺糖缺氧损伤及抑制NMDA受体激活

宋宁宁武继彪魏欣冰管华诗张岫美

Paeonol attenuates oxygen-glucose deprivation injury and inhibits NMDA receptor activation of cultured rat hippocampal neurons

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摘要

摘要:
本研究通过体外培养大鼠海马神经元建立缺糖缺氧损伤 (OGD) 模型, 观察丹皮酚对神经元的保护作用及其对NMDA受体结合活性的抑制作用。原代培养的神经元于建立OGD模型前5 min分别加入丹皮酚及MK-801并观察其作用。OGD模型建立后神经元存活率显著降低, 氨基酸分析仪测得的海马神经元细胞外液兴奋性氨基酸 (EAA) 浓度显著升高, 且海马神经元NMDA受体结合活性及NMDA受体NR1亚基mRNA表达显著增强。而经过丹皮酚及MK-801处理后, 倒置相差显微镜下观察神经元胞体损伤明显减轻, 丹皮酚及MK-801显著降低了细胞死亡率 (P < 0.05) 及细胞外液EAA的升高 (P < 0.05), 并可抑制NMDA受体结合活性的增高及减弱NR1亚基受体mRNA的上调 (P < 0.05)。实验结果表明, 丹皮酚对离体培养的大鼠海马神经元OGD损伤具有保护作用, 其作用机制可能与抑制兴奋性氨基酸升高及影响NMDA受体有关。

Abstract:
The purpose of this study is to determine if paeonol can protect hippocampal neurons against injury due to oxygen-glucose deprivation (OGD) injury. The rat neurons were cultured in an OGD environment and the model of OGD injury was established. Paeonol and MK-801, a positive control drug, were added before deprivation. Neuron viability was measured by the reduction of MTT; glutamate was analyzed by amino acid analyzer; binding activity of NMDA receptor was evaluated by liquid scintillation counting and the expression of NMDA receptor NR1 subunit mRNA was semiquantitatively determined by RT-PCR. Compared with OGD injury group, paeonol treatment obviously increased cell survival rate and reduced the binding activity of NMDA receptors and the release of glutamate; and down-regulating the expression of NR1 subunit. These results suggest that paeonol may exhibit its protective effect against OGD injury by the action on NMDA receptor of rats.

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