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槲皮素、芦丁和黄秋葵(Abelmoschus esculentus Linn.)在地塞米松处理的小鼠中的神经保护作用。

Neuroprotective effects of quercetin, rutin and okra (Abelmoschus esculentus Linn.) in dexamethasone-treated mice.

机构信息

Faculty of Medicine, Mahasarakham University, Mung, Mahasarakham, Thailand.

出版信息

Neurochem Int. 2011 Oct;59(5):677-85. doi: 10.1016/j.neuint.2011.06.014. Epub 2011 Jun 29.

Abstract

The administration of dexamethasone, a synthetic glucocorticoid receptor agonist, causes neuronal death in the CA3 layer of the hippocampus, which has been associated with learning and memory impairments. This study aimed to examine the ability of okra (Abelmoschus esculentus Linn.) extract and its derivatives (quercetin and rutin) to protect neuronal function and improve learning and memory deficits in mice subjected to dexamethasone treatment. Learning and memory functions in mice were examined using the Morris water maze test. The results showed that the mice treated with dexamethasone had prolonged water maze performance latencies and shorter time spent in the target quadrant while mice pretreated with quercetin, rutin or okra extract prior to dexamethasone treatment showed shorter latencies and longer time spent in target quadrant. Morphological changes in pyramidal neurons were observed in the dexamethasone treated group. The number of CA3 hippocampal neurons was significantly lower while pretreated with quercetin, rutin or okra attenuated this change. Prolonged treatment with dexamethasone altered NMDA receptor expression in the hippocampus. Pretreatment with quercetin, rutin or okra extract prevented the reduction in NMDA receptor expression. Dentate gyrus (DG) cell proliferation was examined using the 5-bromo-2-deoxyuridine (BrdU) immunohistochemistry technique. The number of BrdU-immunopositive cells was significantly reduced in dexamethasone-treated mice compared to control mice. Pretreatment with okra extract, either quercetin or rutin was found to restore BrdU-immunoreactivity in the dentate gyrus. These findings suggest that quercetin, rutin and okra extract treatments reversed cognitive deficits, including impaired dentate gyrus (DG) cell proliferation, and protected against morphological changes in the CA3 region in dexamethasone-treated mice. The precise mechanism of the neuroprotective effect of these plant extracts should be further investigated.

摘要

地塞米松(一种合成的糖皮质激素受体激动剂)的给药会导致海马 CA3 层的神经元死亡,这与学习和记忆损伤有关。本研究旨在研究秋葵(Abelmoschus esculentus Linn.)提取物及其衍生物(槲皮素和芦丁)是否能够保护神经元功能并改善接受地塞米松治疗的小鼠的学习和记忆缺陷。使用 Morris 水迷宫测试检查小鼠的学习和记忆功能。结果表明,用地塞米松处理的小鼠水迷宫表现潜伏期延长,而在目标象限花费的时间缩短,而在用地塞米松处理之前用槲皮素、芦丁或秋葵提取物预处理的小鼠潜伏期缩短,在目标象限花费的时间延长。在接受地塞米松治疗的小鼠中观察到锥体神经元的形态变化。CA3 海马神经元的数量明显减少,而用槲皮素、芦丁或秋葵提取物预处理则减轻了这种变化。延长地塞米松治疗改变了海马中的 NMDA 受体表达。用槲皮素、芦丁或秋葵提取物预处理可防止 NMDA 受体表达减少。使用 5-溴-2-脱氧尿苷(BrdU)免疫组织化学技术检查齿状回(DG)细胞增殖。与对照组相比,用地塞米松处理的小鼠的 BrdU-免疫阳性细胞数量明显减少。发现秋葵提取物、槲皮素或芦丁预处理可恢复齿状回中的 BrdU 免疫反应性。这些发现表明,槲皮素、芦丁和秋葵提取物治疗逆转了认知缺陷,包括齿状回(DG)细胞增殖受损,并防止了地塞米松处理的小鼠 CA3 区的形态变化。这些植物提取物的神经保护作用的确切机制应进一步研究。

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