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Ginkgolides protect primary cortical neurons from potassium cyanide-induced hypoxic injury

机译:银杏内酯可保护原代皮层神经元免受氰化钾引起的缺氧损伤

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摘要

In this study, we investigated the effects of ginkgolides (Gins A, B, C and J), the main constituent of the non-flavone fraction of EGb 761, on hypoxic injury induced by potassium cyanide (KCN) in primary cortical neurons. The neurons were pretreated with or without ginkgolides for 24 h before incubation with KCN for 4 h. Cell viability was then determined by a MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyletrazolium bromide] assay and lactate dehydrogenase (LDH) release from neurons into the medium was measured. The morphological changes of neurons were observed under inverse microscopy and electron microscopy. The results demonstrated that KCN (0.05 mmol/l) significantly decreased cell viability and increased LDH release (P < 0.05 versus the control). The characteristic changes of neuronal morphology induced by KCN were observed. However, pretreatment of neurons with 37.5 μg/ml of ginkgolides (ginkgolides + KCN group) led to a significant increase in cell viability, a decrease in LDH release (P < 0.05 versus the KCN group) and a remarkable improvement in cellular morphology in hypoxic neurons compared with the KCN group. The data suggested that ginkgolides have a significant role to protect the primary cortical neurons from hypoxic injury induced by KCN.
机译:在这项研究中,我们调查了银杏内酯(银杏A,B,C和J)(银杏叶761的非黄酮部分的主要成分)对原发皮层神经元中氰化钾(KCN)引起的缺氧损伤的影响。在用KCN孵育4小时之前,先用或不用银杏内酯预处理神经元24小时。然后通过MTT(3- [4,5-二甲基噻唑-2-基] -2,5-二苯基四氮唑溴化物]测定细胞活力,并测定神经元释放的乳酸脱氢酶(LDH)的形态。倒置显微镜和电子显微镜下观察到神经元,结果表明,KCN(0.05 mmol / l)显着降低了细胞活力,增加了LDH的释放(与对照组相比,P <0.05),并观察到了KCN诱导的神经元形态的特征变化。但是,用37.5μg/ ml的银杏内酯(银杏内酯+ KCN组)预处理神经元可导致细胞活力显着增加,LDH释放减少(与KCN组相比,P <0.05)和低氧状态下细胞形态的显着改善。与KCN组相比,银杏内酯对保护原代皮层神经元免受KCN引起的缺氧损伤具有重要作用。

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