Myricetin alleviates pancreatic microcirculation and inflammation in rats with severe acute pancreatitis through FOXO1 and NF-κB pathways

Background Myricetin, a flavonoid, has anti-inflammation effects and can improve pancreatic β cells dysfunction. However, the role of myricetin in severe acute pancreatitis (SAP) and the precise mechanism remain unclear. Objectives This study aimed to investigate how myricetin affects pancreatic damage induced by SAP. Results Myricetin substantially reduced the expression of lipase and amylase, and ameliorated pancreatic damage induced by SAP. Moreover, myricetin inhibited the release of several inflammatory relevant cytokines including tumor necrosis factor alpha (TNF-α), interleukin (IL)-1β, IL-6, and IL-10, alleviated apoptosis of pancreatic alveolar cells, and ameliorated microcirculatory dysfunction in SAP rats. Furthermore, myricetin inhibited the acetylation of forkhead box protein O1(FOXO1) and the phosphorylation of NF-kB. Conclusion Myricetin improves SAP-induced pancreatic injury through suppressing microcirculation dysfunction, overactive inflammatory response, and cell apoptosis. In addition, myricetin deregulates acetylated FOXO1 and phosphorylated nuclear factor kappa B (NF-kB), which may be the potential mechanism for SAP alleviation.