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.



中文翻译：

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Cyanidin-3-O-Glucoside 通过抑制 H2S 调节的 AMPK/mTOR 通路来改善严重急性胰腺炎期间的结肠运动。


背景：花青素-3-O-葡萄糖苷（C3G）是一种重要的花青素，可以调节消化系统功能。与重症急性胰腺炎 (SAP) 相关的炎症会诱导 H ₂ S 产生，从而损害胃肠道 (GI) 系统。我们通过检查 H ₂ S 水平和 AMP 激活蛋白激酶 (AMPK)/哺乳动物雷帕霉素靶点 (mTOR) 通路的活性，研究了 C3G 在减轻 SAP 相关结肠动力丧失中的作用。

方法：采用牛磺胆酸钠诱导SAP大鼠模型，并研究C3G对结肠活动性、H ₂ S产生和炎症反应的影响。检测 AMPK/mTOR 通路变化以评估 H ₂ S 影响 SAP 模型大鼠结肠活动性的通路。通过将结肠肌细胞 (CMC) 置于 C3G、SAP 血浆和 AMPK 激活剂中，进一步检查了 H ₂ S 功能的机制。

结果：给予C3G改善了SAP模型大鼠的结肠运动，但抑制了炎症反应和H ₂ S产生，这与抑制AMPK/mTOR通路有关。此外，即使在施用 C3G 后，激活 CMC 中的 AMPK/mTOR 通路也会促进炎症，但会抑制 Ca2+ 水平。

结论：给予 C3G 可能通过抑制 H ₂ S 介导的 AMPK/mTOR 通路来改善 SAP 相关的结肠活动性。