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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
BACKGROUND: Cyanidin-3-O-glucoside (C3G) is an important anthocyanin that can modulate digestive system functioning. Inflammation associated with severe acute pancreatitis (SAP) induces H(2)S production, which impairs the gastrointestinal (GI) system. We investigated the effects of C3G in attenuatin...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7468407/ https://www.ncbi.nlm.nih.gov/pubmed/32943841 http://dx.doi.org/10.2147/DDDT.S256450 |
Sumario: | BACKGROUND: Cyanidin-3-O-glucoside (C3G) is an important anthocyanin that can modulate digestive system functioning. Inflammation associated with severe acute pancreatitis (SAP) induces H(2)S production, which impairs the gastrointestinal (GI) system. We investigated the effects of C3G in attenuating SAP-associated colonic motility loss by examining the H(2)S 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, H(2)S production, and the inflammatory response was investigated. AMPK/mTOR pathway changes were detected to assess the pathways by which H(2)S influences colonic mobility in SAP-model rats. The mechanism underlying H(2)S 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 H(2)S 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 H(2)S-mediated AMPK/mTOR pathway. |
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