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竹节人参皂苷V通过调节Sirt1/Mn-SOD和GRP78/半胱天冬酶-12通路减轻MPP+诱导的SH-SY5Y细胞神经毒性。

Chikusetsu saponin V attenuates MPP+-induced neurotoxicity in SH-SY5Y cells via regulation of Sirt1/Mn-SOD and GRP78/caspase-12 pathways.

作者信息

Yuan Ding, Wan Jing-Zhi, Deng Li-Li, Zhang Chang-Cheng, Dun Yao-Yan, Dai Yan-Wen, Zhou Zhi-Yong, Liu Chao-Qi, Wang Ting

机构信息

Department of Pharmacology, College of Medical Science, China Three Gorges University, Yichang 443002, China.

Institute of Molecular Biology, China Three Gorges University, Yichang 443002, China.

出版信息

Int J Mol Sci. 2014 Jul 28;15(8):13209-22. doi: 10.3390/ijms150813209.

DOI:10.3390/ijms150813209
PMID:25073091
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4159789/
Abstract

Studies have shown that saponins from Panax japonicus (SPJ) possess neuroprotective effects. However, whether Chikusetsu saponin V (CsV), the most abundant member of SPJ, can exert neuroprotective effects against 1-methyl-4-phenylpyridinium ion (MPP+)-induced cytotoxicity is not known. In this study, we aimed to investigate the neuroprotective effects of CsV on MPP+-induced cytotoxicity in human neuroblastoma SH-SY5Y cells and explore its possible mechanisms. Our results show that CsV attenuates MPP+-induced cytotoxicity, inhibits ROS accumulation, and increases mitochondrial membrane potential dose-dependently. We also found that levels of Sirt1 protein and Mn-SOD mRNA significantly decreased in MPP+-treated group but were restored with CsV treatment in a dose-dependent manner. Furthermore, GRP78 protein and Caspase-12 mRNA levels were elevated by MPP+ exposure but reversed by CsV treatment. CsV inhibited the MPP+-induced downregulation of Bcl-2 and up-regulation of Bax in a dose-dependent manner and, thus, increased the ratio of Bcl-2/Bax. Overall, these results suggest that Sirt1/Mn-SOD and GRP78/Caspase-12 pathways might be involved in the CsV-mediated neuroprotective effects.

摘要

研究表明，竹节参皂苷（SPJ）具有神经保护作用。然而，作为SPJ中含量最丰富的成分，竹节参皂苷V（CsV）是否能对1-甲基-4-苯基吡啶离子（MPP+）诱导的细胞毒性发挥神经保护作用尚不清楚。在本研究中，我们旨在探讨CsV对MPP+诱导的人神经母细胞瘤SH-SY5Y细胞毒性的神经保护作用，并探索其可能的机制。我们的结果表明，CsV可减轻MPP+诱导的细胞毒性，剂量依赖性地抑制活性氧（ROS）积累，并增加线粒体膜电位。我们还发现，在MPP+处理组中，Sirt1蛋白和锰超氧化物歧化酶（Mn-SOD）mRNA水平显著降低，但经CsV处理后呈剂量依赖性恢复。此外，MPP+暴露可使葡萄糖调节蛋白78（GRP78）蛋白和半胱天冬酶12（Caspase-12）mRNA水平升高，但CsV处理可使其逆转。CsV剂量依赖性地抑制MPP+诱导的Bcl-2下调和Bax上调，从而增加Bcl-2/Bax比值。总体而言，这些结果表明，Sirt1/Mn-SOD和GRP78/Caspase-12通路可能参与了CsV介导的神经保护作用。

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