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首页> 外文期刊>Drug Design, Development and Therapy >Cyanidin-3-O-Glucoside Improves Colonic Motility During Severe Acute Pancreatitis by Inhibiting the H 2 S-Regulated AMPK/mTOR Pathway
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Cyanidin-3-O-Glucoside Improves Colonic Motility During Severe Acute Pancreatitis by Inhibiting the H 2 S-Regulated AMPK/mTOR Pathway

机译：Cyanidin-3-O-葡糖苷通过抑制H 2 S调节的AMPK / MTOR途径而改善了严重急性胰腺炎的结肠运动性

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Background: Cyanidin-3-O-glucoside (C3G) is an important anthocyanin that can modulate digestive system functioning. Inflammation associated with severe acute pancreatitis (SAP) induces H2S production, which impairs the gastrointestinal (GI) system. We investigated the effects of C3G in attenuating SAP-associated colonic motility loss by examining the H2S level and activity of AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway. Methods: A rat model of SAP was induced using sodium taurocholate, and the effect of C3G on colonic mobility, H2S production, and the inflammatory response was investigated. AMPK/mTOR pathway changes were detected to assess the pathways by which H2S influences colonic mobility in SAP-model rats. The mechanism underlying H2S function was further examined by subjecting colonic muscle cells (CMCs) to C3G, SAP plasma and an AMPK activator. Results: Administering C3G improved colonic motility but suppressed the inflammatory response and H2S production in the SAP-model rats, which was associated with inhibiting the AMPK/mTOR pathway. Furthermore, activating the AMPK/mTOR pathway in CMCs promoted inflammation but suppressed Ca2 levels, even after administering C3G. Conclusion: Administering C3G may improve SAP-associated colonic mobility by inhibiting the H2S-mediated AMPK/mTOR pathway.
机译：背景：Cyanidin-3-O-葡糖苷（C3G）是一种重要的花青素，可以调节消化系统功能。与严重急性胰腺炎（SAP）相关的炎症诱导H2S生产，损害胃肠道（GI）系统。我们研究了C3G通过检查雷帕霉素（MTOR）途径的AMP活化蛋白激酶（AMPK）/哺乳动物靶标的活性和活性来衰减SAP相关结肠运动损失。方法：使用牛磺酸钠诱导SAP的大鼠模型，研究C3G对结肠迁移率，H2S生产和炎症反应的影响。检测AMPK / MTOR途径变化以评估H2S在SAP模型大鼠中影响结肠流动性的途径。通过使结肠肌细胞（CMC），SAP等离子体和AMPK活化剂进行结肠肌细胞（CMC）来进一步检查H 2 S功能的机制。结果：施用C3G改善的结肠运动，但抑制了SAP模型大鼠中的炎症反应和H2S产生，其与抑制AMPK / mTOR途径相关。此外，即使在施用C3G后，也会激活CMCS中的AMPK / mTOR途径促进炎症但抑制CA2水平。结论：通过抑制H 2 S介导的AMPK / MTOR途径，施用C3G可以改善SAP相关的结肠迁移率。

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