Neuroprotective effects of ginseng pectin through the activation of ERK/MAPK and Akt survival signaling pathways
Neuroprotective effects of ginseng pectin through the activation of ERK/MAPK and Akt survival signaling pathways
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人参果胶通过激活 ERK/MAPK 和 Akt 存活信号通路的神经保护作用
DOI：
10.3892/mmr.2012.811
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发表时间：
2012-05-01
影响因子：
3.4
通讯作者：
Zhou, Yifa
中科院分区：
文献类型：
--
作者：
Fan, Yuying;Sun, Chengxin;Zhou, Yifa
在这项研究中，我们研究了人参果胶（GP）对过氧化氢（H2 O2）诱导的不同神经元细胞神经元毒性的神经保护活性。GP选择性地减弱H2 O2诱导的原代皮层神经元细胞和人胶质母细胞瘤U87细胞损伤达26%。H2 O2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保持细胞的完整性和减少核凝聚。Western blot分析结果显示，GP预处理可增加皮层神经元细胞外信号调节激酶1和2（ERK 1/2）及Akt的磷酸化水平。U87细胞ERK 1/2磷酸化水平升高，Akt磷酸化水平降低。这些结果表明，GP对H2 O2诱导的细胞凋亡的保护作用可能是由于ERK 1/2和Akt的磷酸化的激活，然而，所涉及的机制取决于不同的细胞系。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。
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 glioblastorna U87 cells. Following H2O2 exposure, DAPI staining and neuron-specific beta-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.