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灵芝酸对海马神经元癫痫样放电的影响:基于脑源性神经营养因子、瞬时受体电位阳离子通道蛋白3及细胞凋亡改变的见解

Effects of ganoderic acids on epileptiform discharge hippocampal neurons: insights from alterations of BDNF,TRPC3 and apoptosis.

作者信息

Yang Zhi-wei, Wu Fei, Zhang Sheng-Li

出版信息

Pharmazie. 2016 Jun;71(6):340-4.

Abstract

Recently, Ganoderma lucidum spores (GLS) have shown anti-epileptic effects. However, there are no reports on the anti-epileptic effects of its chemical constituents ganoderic acids (GAs), and more research is needed to better understand the mechanism of GLS activity. In this work, rat primary hippocampal neurons in an in vitro model were used to assess the intervention effects of GAs on epileptiform discharge hippocampal neurons and expression of both BDNF and TRPC3, with the aid of immunofluorescence, MTT method and flow cytometry. It was found that BDNF and TRPC3 are expressed in all cells and were mainly localized in the cytoplasm. The fluorescence intensities of BDNF and TRPC3 in GAs groups were higher than those of normal control and model groups, especially at 80 μg/ml (P < 0.05). The apoptosis rate of neurons was inversely proportional to BDNF and TRPC3 changes (P < 0.01). Therefore, BDNF and TRPC3 should be involved in the occurrence and development of epilepsy. GAs might indirectly inhibit mossy fiber sprouting and adjust the synaptic reconstructions by promoting the expression of BDNF and TRPC3. Besides, GAs could exert a protective effect on hippocampal neurons by promoting neuronal survival and the recovery of injured neurons.

摘要

最近,灵芝孢子(GLS)已显示出抗癫痫作用。然而,关于其化学成分灵芝酸(GAs)的抗癫痫作用尚无报道,需要更多研究以更好地理解GLS活性机制。在这项工作中,借助免疫荧光、MTT法和流式细胞术,使用体外模型中的大鼠原代海马神经元来评估GAs对癫痫样放电海马神经元以及BDNF和TRPC3表达的干预作用。结果发现,BDNF和TRPC3在所有细胞中均有表达,且主要定位于细胞质中。GAs组中BDNF和TRPC3的荧光强度高于正常对照组和模型组,尤其是在80μg/ml时(P<0.05)。神经元凋亡率与BDNF和TRPC3的变化呈负相关(P<0.01)。因此,BDNF和TRPC3应参与癫痫的发生和发展。GAs可能通过促进BDNF和TRPC3的表达间接抑制苔藓纤维出芽并调节突触重建。此外,GAs可通过促进神经元存活和损伤神经元的恢复对海马神经元发挥保护作用。

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