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.
Conclusion
Administering C3G may improve SAP-associated colonic mobility by inhibiting the H2S-mediated AMPK/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.