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首页> 外文期刊>Cellular Physiology and Biochemistry >Application of iTRAQ-Based Quantitative Proteomics Approach to Identify Deregulated Proteins Associated with Liver Toxicity Induced by Polygonum Multiflorum in Rats
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Application of iTRAQ-Based Quantitative Proteomics Approach to Identify Deregulated Proteins Associated with Liver Toxicity Induced by Polygonum Multiflorum in Rats

机译：基于iTRAQ的定量蛋白质组学方法在何首乌诱导的大鼠肝毒性相关蛋白中的调控研究

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>Background/Aims: Clinical reports on adverse reactions that result from Polygonum multiflorum (PM) and its preparations, especially regarding liver injury, have recently received widespread attention. This study aimed to investigate the mechanism of hepatotoxicity induced by different PM extracts through iTRAQ quantitative proteomics. Methods: The different PM extracts were orally administrated for 90 days to rats, and the hepatotoxicity effect was evaluated through measurement of biochemical indexes, oxidative damage indexes and hematoxylin-eosin (HE) staining. Then, the hepatotoxicity mechanism was investigated by iTRAQ quantitative proteomics. Results: The results of biochemical and histopathological analyses showed that liver injury occurred in all groups of rats given by various PM extracts, which proved all of the PM extracts could induce hepatotoxicity. The hepatotoxicity mechanism may differ between the total extract group and the other groups through the results of biochemical indicators. The iTRAQ proteomics study showed that hepatotoxicity resulting from PM was mainly related to the abnormal activity of mitochondrion function-related oxidative phosphorylation pathways. Conclusion: This iTRAQ proteomics study revealed that the hepatotoxicity induced by PM is primarily related to the oxidative phosphorylation pathways. NADH dehydrogenase family proteins and Slc16a2 could be potential biomarkers of hepatotoxicity resulting from PM.
机译：> 背景/目标： 最近，关于何首乌及其制剂引起的不良反应的临床报道，尤其是关于肝损伤的报道。本研究旨在通过iTRAQ定量蛋白质组学研究不同PM提取物诱导的肝毒性机制。 方法： 将不同的PM提取物口服给予大鼠90天，并通过测量生化指标，氧化损伤指标和苏木精-曙红（HE）评估其肝毒性作用。 ）染色。然后，通过iTRAQ定量蛋白质组学研究了肝毒性机制。 结果： 生化和组织病理学分析结果表明，各种PM提取物对所有组的大鼠均发生肝损伤，证明所有PM提取物均可以诱导肝毒性。通过生化指标的结果，总提取物组和其他组之间的肝毒性机制可能有所不同。 iTRAQ蛋白质组学研究表明，PM引起的肝毒性主要与线粒体功能相关的氧化磷酸化途径的异常活性有关。 结论： 这项iTRAQ蛋白质组学研究表明，PM引起的肝毒性主要与氧化磷酸化途径有关。 NADH脱氢酶家族蛋白和 Slc16a2 可能是PM引起的肝毒性的潜在生物标志物。

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