School of Life Sciences, Northeast Normal University, Changchun, Jilin 130024, PR China.
Mol Med Rep. 2012 May;5(5):1185-90. doi: 10.3892/mmr.2012.811. Epub 2012 Feb 28.
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.
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。
