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人参果胶通过激活 ERK/MAPK 和 Akt 存活信号通路发挥神经保护作用。

Neuroprotective effects of ginseng pectin through the activation of ERK/MAPK and Akt survival signaling pathways.

机构信息

School of Life Sciences, Northeast Normal University, Changchun, Jilin 130024, PR China.

出版信息

Mol Med Rep. 2012 May;5(5):1185-90. doi: 10.3892/mmr.2012.811. Epub 2012 Feb 28.

Abstract

In this study, we investigated the neuroprotective activities of ginseng pectin (GP) against hydrogen peroxide (H2O2)-induced neuronal toxicity in different neuronal cells. GP selectively attenuated H2O2-induced damage up to 26% in primary cortical neuron cells and human glioblastoma U87 cells. Following H2O2 exposure, DAPI staining and neuron-specific β-tubulin antibody probing indicated that GP maintained cell integrity and decreased nuclei condensation. Data from western blot analysis revealed that pre-treatment with GP increased the phosphorylation of both the extracellular signal-regulated kinases 1 and 2 (ERK1/2) and Akt in cortical neuron cells. However, the phosphorylation of ERK1/2 was increased, but that of Akt was decreased in U87 cells. These results suggest that the protective effects of GP against H2O2-induced apoptosis may be due to the activation of the phosphorylation of ERK1/2 and Akt; however, the mechanisms involved differ depending on the cell line. This neuroprotective property indicates that GP could serve as a potential therapeutic agent for neurodegenerative diseases.

摘要

在这项研究中,我们研究了人参果胶(GP)对不同神经元细胞中海氧自由基(H2O2)诱导的神经元毒性的神经保护活性。GP 选择性地减轻了原代皮质神经元细胞和人胶质母细胞瘤 U87 细胞中高达 26%的 H2O2 诱导的损伤。在 H2O2 暴露后,DAPI 染色和神经元特异性β-微管蛋白抗体探测表明 GP 保持了细胞完整性并减少了核浓缩。来自 Western blot 分析的数据表明,在用 GP 预处理后,皮质神经元细胞中细胞外信号调节激酶 1 和 2(ERK1/2)和 Akt 的磷酸化均增加。然而,在 U87 细胞中,ERK1/2 的磷酸化增加,但 Akt 的磷酸化减少。这些结果表明,GP 对 H2O2 诱导的细胞凋亡的保护作用可能归因于 ERK1/2 和 Akt 的磷酸化的激活;然而,所涉及的机制因细胞系而异。这种神经保护特性表明,GP 可以作为神经退行性疾病的潜在治疗剂。

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