Background: Acute pancreatitis (AP) is a common inflammatory disease that may develop to severe AP (SAP), resulting in life-threatening complications. Impaired autophagic flux is a characteristic of early AP, and its accumulation could activate oxidative stress and nuclear factor κB (NF-κB) pathways, which aggravate the disease process.
Aim: To explore the therapeutic effects of regulating autophagy after the onset of AP.
Methods: In this study, intraperitoneal injections of 3-methyladenine (3-MA) and rapamycin (RAPA) in the L-arginine or cerulein plus lipopolysaccharide (LPS) Balb/C mouse model. At 24 h after the last injection, pulmonary, intestinal, renal and pancreatic tissues were analyzed.
Results: We found that 3-MA ameliorated systemic organ injury in two SAP models. 3-MA treatment impaired autophagic flux and alleviated inflammatory activation by modulating the NF-κB signaling pathway and the caspase-1-IL-1β pathway, thus decreasing the injuries to the organs and the levels of inflammatory cytokines.
Conclusion: Our study found that the regulation of autophagy could alter the progression of AP induced by L-arginine or cerulein plus LPS in mice.
Keywords: 3-methyladenine; Acute pancreatitis; Autophagy; Inflammatory.