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首页> 外文期刊>RSC Advances >iTRAQ-based quantitative proteomic analysis for identification of biomarkers associated with emodin against severe acute pancreatitis in rats
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iTRAQ-based quantitative proteomic analysis for identification of biomarkers associated with emodin against severe acute pancreatitis in rats

机译：基于ITRAQ的定量蛋白质组学分析，用于鉴定与大鼠严重急性胰腺炎的癌症相关的生物标志物

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In the present work, we investigated the action of emodin against rats with severe acute pancreatitis (SAP) induced by administering 5% sodium taurocholate. The results demonstrated that emodin markedly decreased plasma amylase, lipase, IL-1β, IL-6 and TNF-α activities. Immunohistochemistry and immunofluorescence results indicated that emodin down-regulated MPO protein expression. Meanwhile, emodin improved pancreatic histopathology and acinous cell ultrastructure. In addition, real-time PCR results also proved that emodin significantly inhibited IL-1β, IL-6 and TNF-α mRNA expression. Finally, a total of 32 differentially expressed proteins from rat pancreas in response to stimulus were discovered by using iTRAQ-based quantitative proteomic analysis. These proteins were related to each other and involved in different biological processes. Among them, a new biomarker, HTRA1, was found to associate with SAP, which was validated by western blot. Further work found, for the first time, that proteins in the HTRA1/TGF-β1 signaling cascade including HTRA1, TGF-β1, IL-33, MyD88, TRAF6 and NF-κB were involved in the mechanisms of emodin against SAP. Ultimately, our results suggested that emodin had potent actions against SAP injury by inhibiting the HTRA1/TGF-β1 signaling pathway and subsequent inflammatory responses. These findings provide new insights that will aid in illuminating the action of emodin against SAP insult.
机译：在目前的工作中，我们研究了大黄素对大鼠的作用对通过施用5％牛磺酸钠诱导的严重急性胰腺炎（SAP）的作用。结果表明，大蛋白显着降低了血浆淀粉酶，脂肪酶，IL-1β，IL-6和TNF-α活性。免疫组织化学和免疫荧光结果表明大黄素下调的MPO蛋白表达。同时，大黄素改善了胰腺组织病理学和致铬细胞超微结构。此外，实时PCR结果还证明了大蛋白显着抑制IL-1β，IL-6和TNF-αmRNA表达。最后，通过使用基于ITRAQ的定量蛋白质组学分析，发现了响应于刺激的大鼠胰腺的32种差异表达蛋白。这些蛋白质彼此相关并参与不同的生物过程。其中，发现新的生物标志物HTRA1与SAP联系起来，这些污染污染验证。首次找到进一步的工作，即，包括HTRA1，TGF-β1，IL-33，MYD88，TRAF6和NF-κB的HTRA1 / TGF-β1信号传导级联中的蛋白参与大黄素对SAP的机制。最终，我们的结果表明，通过抑制HTRA1 / TGF-β1信号通路和随后的炎症反应，大黄素对SAP损伤具有有效的作用。这些调查结果提供了新的见解，有助于照亮大蛋白对SAP侮辱的动作。

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