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首页> 外文期刊>RSC Advances >Sphingolipidomic study of davidiin-treated HepG2 human hepatocellular carcinoma cells using UHPLC-MS
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Sphingolipidomic study of davidiin-treated HepG2 human hepatocellular carcinoma cells using UHPLC-MS

机译：使用UHPLC-MS研究达维丁素处理的HepG2人肝癌细胞的鞘脂代谢

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摘要

Davidiin, a natural product originating from Polygonum capitatum, has been proven to possess anti-hepatocellular carcinoma activity. To explore the mechanisms underlying the activity of davidiin, sphingolipids (SPLs) in HepG2 human hepatocellular carcinoma cells with or without the treatment of davidiin were comprehensively analyzed using an improved sphingolipidomic approach established in our lab. A total of 133 SPLs were identified and quantified by using the multiple reaction monitoring (MRM) technique. The results revealed an extensive elevation of dihydroceramide (DHCer) and sphinganine (Sa) induced by davidiin in HepG2 cells, which potentially mediate the cytotoxicity of davidiin. Based on the alteration of upstream and downstream products in the biosynthesis and metabolism network of SPLs, the elevated DHCer and Sa are proposed to result from the inhibition effect of davidiin on dihydroceramide desaturase (DES), which was further confirmed by in vitro assay. Given the emerging role of DES as a therapeutic target of cancer, our results not only provided evidence for the mechanisms underlying the cytotoxicity of davidiin, but also underscored the potential of ellagitannin as a new group of aromatic natural products acting on DES.
机译：大黄素（Davidiin）是一种来自 Polygonum capitatum 的天然产物，已被证明具有抗肝细胞癌活性。为了探索达维丁的活性的潜在机制，我们使用在我们实验室中建立的改进的鞘脂血脂学方法，对有或没有达维丁的HepG2人肝癌细胞中的鞘脂（SPL）进行了全面分析。使用多反应监测（MRM）技术鉴定并定量了总共133个SPL。结果显示达维丁在HepG2细胞中诱导了二氢神经酰胺（DHCer）和鞘氨醇（Sa）的广泛升高，这可能介导了达维丁的细胞毒性。基于SPLs生物合成和代谢网络中上游和下游产物的变化，提出DHCer和Sa的升高是由于达维丁对二氢神经酰胺去饱和酶（DES）的抑制作用所致，这在体外进一步得到证实。 分析。考虑到DES作为癌症治疗靶点的新兴作用，我们的研究结果不仅为达维丁的细胞毒性机制提供了证据，而且强调了鞣花单宁作为一类新的作用于DES的芳香族天然产物的潜力。

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