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Cyanidin-3-O-Glucoside Improves Colonic Motility During Severe Acute Pancreatitis by Inhibiting the H2S-Regulated AMPK/mTOR Pathway.
Drug Design, Development and Therapy ( IF 4.7 ) Pub Date : 2020-08-19 , DOI: 10.2147/dddt.s256450
Wei Lian 1 , Wensheng Chen 1
Affiliation  

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:


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。

更新日期:2020-08-19
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