Table8_Protective Effect of Dictyophora Polysaccharides on Sodium Arsenite-Induced Hepatotoxicity: A Proteomics Study.XLSX

The purpose of this study is to understand the mechanism of sodium arsenite (NaAsO2)-induced apoptosis of L-02 human hepatic cells, and how Dictyophora polysaccharide (DIP) protects L-02 cells from arsenic-induced apoptosis. The results revealed that DIP pretreatment inhibited NaAsO2 induced L-02 cells apoptosis by increasing anti-apoptotic Bcl-2 expression and decreasing pro-apoptotic Bax expression. Proteomic analysis showed that arsenic treatment disrupted the expression of metabolism and apoptosis associated proteins, including ribosomal proteins (RPs). After pretreatment with DIP, the expression levels of these proteins were reversed or restored. For the first time, it was observed that the significant decrease of cytoplasmic RPs and the increase of mitochondrial RPs were related to human normal cell apoptosis induced by arsenic. This is also the first report that the protective effect of DIP on cells was related to RPs. The results highlight the relationship between RPs and apoptosis, as well as the relationship between RPs and DIP attenuating arsenic-induced apoptosis.

本研究旨在阐明亚砷酸钠（sodium arsenite, NaAsO2）诱导L-02人肝细胞凋亡的分子机制，以及竹荪多糖（Dictyophora polysaccharide, DIP）对砷诱导肝细胞凋亡的保护作用及其机制。研究结果显示，DIP预处理可通过上调抗凋亡蛋白Bcl-2的表达、下调促凋亡蛋白Bax的表达，抑制NaAsO2诱导的L-02细胞凋亡。蛋白质组学分析表明，砷处理会扰乱代谢相关与凋亡相关蛋白的表达，其中包括核糖体蛋白（ribosomal proteins, RPs）。经DIP预处理后，上述蛋白的表达水平可被逆转或恢复至正常水平。本研究首次观测到，细胞质核糖体蛋白水平显著降低、线粒体核糖体蛋白水平升高，与砷诱导的人正常细胞凋亡密切相关；同时也是首次报道DIP的细胞保护作用与核糖体蛋白相关。本研究结果进一步凸显了核糖体蛋白与细胞凋亡之间的关联，以及核糖体蛋白在DIP缓解砷诱导细胞凋亡过程中的作用。