Cyanidin-3-O-glucoside (C3G) is an important anthocyanin that can modulate digestive system functioning. Inflammation associated with severe acute pancreatitis (SAP) induces H 2S production, which impairs the gastrointestinal (GI) system. We investigated the effects of C3G in attenuating SAP-associated colonic motility loss by examining the H 2S level and activity of AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway.
A rat model of SAP was induced using sodium taurocholate, and the effect of C3G on colonic mobility, H 2S production, and the inflammatory response was investigated. AMPK/mTOR pathway changes were detected to assess the pathways by which H 2S influences colonic mobility in SAP-model rats. The mechanism underlying H 2S function was further examined by subjecting colonic muscle cells (CMCs) to C3G, SAP plasma and an AMPK activator.
Administering C3G improved colonic motility but suppressed the inflammatory response and H 2S 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.